Feeling cold (because in American buildings the air conditioning is set at only 16 degrees) and hungry (because there you can only have fast food and American coffee, which is rainwater for Europeans) – I watched in amazement a workshop conducted by 3 top professors come to prove that soft drinks are healthier than water.

The truth being told, only the first two professors did the job they’ve been payed to do bringing seemingly scientific arguments to prove (- I still wonder today: To God damn whom?!) that cola is better for humans than water. The third one, a little younger than the others and a little more Tarzan, broke down their pseudo-scientific arguments, dismantling them one by one.

I still remember with deep pleasure the organizers face color standing on the sidelines of the room, changing from the pink bon-bon delighted by the first two presentations to the brown-cola during the third. Well …  the face of the first two presenters also turned brown-cola during the third presentation, but what the hell they were thinking ?!

Theoretically, any mentally healthy person with or without a degree in nutrition would be shocked to attend an international nutrition workshop designed to prove that you become healthier if you drink cola than if you drink water. The fact that you are a top professor saying stupidities does not change the stupidities, it only changes your image as an impartial expert putting the spotlight on the fact that you are now for sale.

Neither light soda drinks nor those with sugars provide the body with actual sugar, but with all kinds of synthetic substances, generating: weight gain, dyslipidemia, hepatic and renal steatosis and an appetite disturbed enough to create a continuous craving that makes you want to to consume them every damn day.

Now, if you’re wondering what the hell was I thinking to attend such a workshop, I must mention two sad but essential conference aspects:

1. The food served at nutrition conferences varies from extremely bad, to bad, to purely inedible, depending on the budget and the organizers’ equanimity towards the conference participants.
2. And one of the conferences with the worst food on the planet is the annual conference organized by the American Nutrition Society, which is why the focus of many of the 30,000 participants moves around lunch to identify the workshops organized by various companies that promote their products.

These big conferences take place for days in a row, continuously from 8 in the morning to 8 in the evening, and if you don’t want to starve at noon you quietly sit and attend one of the many elegantly veiled commercials called “workshop” to have access to something to eat that is somewhat edible.

Watching these commercials placed in the middle of conferences is like watching commercials placed in a good movie. Theoretically you can go to the kitchen at any time to eat in a civilized manner, but practically you risk losing important presentations strategically placed throughout the program to keep you at the conference.

Two years later, in the cozy comfort of my home, I relive the same shock while reading the French study which raises the hypothes about how nicotine protects us from respiratory disease Covid-19 just as I was shocked then by the lovely studies meant to prove that cola protects us from obesity and metabolic diseases.

I would like to quote this study, but it is only published as a preprint in some journal and already republished after various international researches asked for more details about the data behind the puzzling conclusion.

It is basically a statistical analysis that calculates the incidence of coronavirus infection compared between those who report smoking and those who are officially known to smoke.

Coronavirus-infected people admitted to a hospital in France between 28 February and 30 March 2020 (considered patients with severe infection) are taken together with those consulted in the same hospital between 23 March and 9 April (considered patients with mild or moderate infection) and asked, “Do you smoke?”

Those who answered yes were labeled “smokers”.

Those who answered no were labeled “non-smokers”.

Just that you can answer exactly how your panic dictates when you’re asked whether you smoke or not in the midst of a pandemic of a respiratory disease.

The studies that assess the real impact of smoking on human health don’t just consider the answers yes or no as enough evidence to actually know the smoking status of a person. Objectively, the smoking status is attested by blood and urine tests that show the metabolic evidence that a person smokes or not. (1)

Obviously, these studies are more difficult to do, and in the midst of the pandemic there is no time for such details, so the people surveyed in the French observational study were not tested in any way to assess whether the answer about their smoking is real.

But without the metabolic verification of the given answer, one can respond whatever they might consider appropriate.

If you say you don’t smoke you don’t risk anyone blaming you for taking up the coronavirus infection, you don’t risk not being treated well because how the hell do you still smoke when you were repeatedly warned not to touch your mouth with your hand until after you washed it 15 times, and you don’t risk someone slapping you in the midst of a panic pandemic.

If you say you don’t smoke even if you smoke since you were 16, you can now remain calm, you are officially a non-smoker, and you get to be treated like any other human being because it is not your fault, you did nothing wrong to get the respiratory infection.

And tam-taram-ta-dam-dam-dam… the number of those infected with coronavirus who admitted to smoking is only 5.3% compared to the 25.4% who are officially known to smoke in France.

So, tam-taram-ta-dam-dam-dam… Breaking News: Covid-19 incidence is lower in smokers!

The authors of the study officially regret that the number of the study participant was lowered by the fact that they were not allowed access to intensive care units, considering that the protective effect of smoking would have been much more clearly highlighted if they had been allowed to ask intubated patients if they smoke or not …

Trying to prove that drinking cola improves your health at one of the largest international nutrition conferences feels as stupefying as trying to prove that nicotine protects you during a pandemic of infectious respiratory disease.

We witness in dismay the leaders of the planet flow of intelligence.

From the herd immunity proposed by the English boss, to the disinfectant injections proposed by the American boss, to sex as a method of maintaining mental health proposed by the Danish boss, somehow it also had to come to smoking.

At the moment they are a little busy dealing with all this pandemic to have the time to investigate whether the beneficial effects cola has against obesity and diabetes also protects us against Covid-19. Let’s have a little patience, after they’ll finish with the immunity from the holy spirit, the disinfectant injections, the sex and the smoking they will probably end up researching the cola benefits too.

Relaxingly smoking they cigarettes while surfing the corona wave, pseudo-researchers issue hypotheses after hypotheses, one more crazy and less scientific than the other.

And how on Earth to issue hypotheses than from a study…

But “study” is a word as vague as the word “human”.

There are humans and humans, there are studies and studies. Not that they are good or bad, but at least their training level and expertise can differ:

• first graders use the same letters as doctors – all being named using the same word “human” and theoretically any first grader has the potential to become a doctor
• observational studies use the same letters as randomized controlled clinical trials – all being called using the same word “study” and theoretically any observational study has the potential to become a randomized controlled clinical trial

Just that most children do not become doctors, and that most observational studies do not become randomized controlled clinical trials.

Still – because it was written in a “study” – the internet roars with all kinds of miracles, one more startling than the otter.

But, although the fact that it comes from a “study” seems like enough of an argument if you don’t know how to evaluate the degree of clinical validity of a study, one observational study does not wipe out all we already know about the harms inflicted by smoking.

When a kindergarten study comes to tell us that smoking protects us from respiratory infections, it would be logical to call an adult study to explain to the kid that:

1. smoking increases the risk of respiratory infections and nosocomial complications resulting in increased respiratory mucosal permeability to pathogens, local inflammation and decreased immunity (2)
2. smokers with respiratory infections have an increased risk of developing more severe disease (3)
3. smoking increases the risk of diseases associated with a severe evolution or death in those infected with coronavirus:
   • smoking increases the risk of cardiovascular disease, (4) including in non-smokers exposed to second-hand smoke (5) and in smokers of e-cigarettes (6) and in those smoking hookah (7)
   • smoking increases the risk of chronic kidney disease in direct proportion to the number of cigarettes smoked per day and to the years since you’ve been smoking, dialysis being less effective in patients with advanced kidney disease who continue to smoke (8, 9, 10)
   • smoking increases the risk of diabetes even in non-smokers exposed at home to secondhand smoke, associating hyperglycaemia, increased HbA1c and dyslipidemia (11, 12, 13)

Over 1 billion people are known to smoke globally, and maybe in the midst of today’s pandemic it would be good to calm them down, so they can continue to calm themselves down through smoking.

But it is not only about the fact that smoking increases the risk of respiratory infectious diseases, about the fact that smokers have worse prognostics when they get these respiratory infectious diseases, or about the fact that smoking increases the the risk of diseases associated with a severe evolution or death in those infected with coronavirus: cardiovascular disease, kidney disease, and diabetes.

On top of these, smoking also increases the risk of chronic lung disease in direct proportion to the time you smoke. (14, 15) And once hospitalized, the simple fact that you already have a chronic lung disease increases your risk of in hospital mortality by 10%. (16)

Even in the case of coronavirus infection, the systematic analysis of the few studies available today shows an increased risk of severe Covid-19 infection in people with chronic lung disease who continue to smoke. (17)

The number of annual deaths from chronic lung disease has increased globally from 3.32 million in 1990 to 3.91 million in 2017. (18)

On average, over 3 million people die each year from chronic lung diseases associated with smoking.

Today, 28 April, at a global level 216.281 people died with Covid-19. We don’t even know the number of deaths actually caused by coronavirus; we only know that these people also had Covid-19 while dying.

And still, studies promoting smoking against a respiratory disease sprung in full pandemic… Or maybe just the nicotine… We can’t say for sure, but maybe it’s just the nicotine…

Despite today’s bombastic “breaking news”, people don’t die only from Covid-19.

Promoting nicotine in today’s pandemic of respiratory infection spells stupidity just like promoting soda drinks in today’s pandemic of diabetes and obesity.

Although the mental fog globally induced by panic has dramatically increased the need for magic solutions, smoking amplifies all know factors associated with severe evolution and death in those infected with coronavirus

– But if the smart ones of the planet say differently?!

You look amazed at how the boss makes smoke rolls, relaxed, knowing he’s right because he’s the boss, and you are not because you’re not.

Just that the magic of being right because you’re the boss only applies to humans, the virus doesn’t make such faible differences.

And although it seems that money can buy health regardless of your behaviour, the boss countries that globally lead us today are the most affected ones – both by the pandemic of obesity and metabolic diseases, and by the pandemic of coronavirus.

Thus, regardless of what the boss says, for your health, use your own brain and common sense.

Scientific references:

(1) Martin, Elizabeth M., et al. “E-cigarette use results in suppression of immune and inflammatory-response genes in nasal epithelial cells similar to cigarette smoke.” American Journal of Physiology-Lung Cellular and Molecular Physiology 311.1 (2016): L135-L144.

(2) Bagaitkar, Juhi, Donald R. Demuth, and David A. Scott. “Tobacco use increases susceptibility to bacterial infection.” Tobacco induced diseases 4.1 (2008): 12.

(3) Han, Lefei, et al. “Smoking and influenza-associated morbidity and mortality: a systematic review and meta-analysis.” Epidemiology 30.3 (2019): 405-417.

(4) King, Cecile C., et al. “Longitudinal impact of smoking and smoking cessation on inflammatory markers of cardiovascular disease risk.” Arteriosclerosis, thrombosis, and vascular biology 37.2 (2017): 374-3

(5) Attard, Ritienne, et al. “The impact of passive and active smoking on inflammation, lipid profile and the risk of myocardial infarction.” Open Heart 4.2 (2017): e000620.

(6) Carnevale, Roberto, et al. “Acute impact of tobacco vs electronic cigarette smoking on oxidative stress and vascular function.” Chest 150.3 (2016): 606-612.

(7) Bhatnagar, Aruni, et al. “Water pipe (hookah) smoking and cardiovascular disease risk: a scientific statement from the American Heart Association.” Circulation 139.19 (2019): e917-e936.

(8) Roehm, Bethany, et al. “Cigarette smoking attenuates kidney protection by angiotensin-converting enzyme inhibition in nondiabetic chronic kidney disease.” American journal of nephrology 46.4 (2017): 260-267.

(9) Zhang, Shu Tong, et al. “Effects of Smoking on Chronic Kidney Disease.” J Am Soc Nephrol 21.11 (2019): 1819-1834.

(10) Trajceska, Lada, et al. “Active Smoking is Associated with Lower Dialysis Adequacy in Prevalent Dialysis Patients.” Open Access Macedonian Journal of Medical Sciences 7.21 (2019).

(11) Akter, Shamima, Atsushi Goto, and Tetsuya Mizoue. “Smoking and the risk of type 2 diabetes in Japan: a systematic review and meta-analysis.” Journal of epidemiology 27.12 (2017): 553-561.

(12) Maddatu, Judith, Emily Anderson-Baucum, and Carmella Evans-Molina. “Smoking and the risk of type 2 diabetes.” Translational Research 184 (2017): 101-107.

(13) Gu, Lijuan, et al. “Effects of Passive Smoking on Glycemic Parameters and Lipid Profiles in a Chinese Female Population.” Clinical laboratory 63.7 (2017): 1147-1152.

(14) Jayes, Leah, et al. “SmokeHaz: systematic reviews and meta-analyses of the effects of smoking on respiratory health.” Chest 150.1 (2016): 164-179.

(15) Liu, Yong, et al. “Smoking duration, respiratory symptoms, and COPD in adults aged≥ 45 years with a smoking history.” International journal of chronic obstructive pulmonary disease 10 (2015): 1409.

(16) Sin, Don D. “Contemporary concise review 2019: chronic obstructive pulmonary disease.” Respirology 104 (2020).

(17) Zhao, Qianwen, et al. “The impact of COPD and smoking history on the severity of Covid‐19: A systemic review and meta‐analysis.” Journal of Medical Virology (2020).

(18) Li, Xiaochen, et al. “Trends and risk factors of mortality and disability adjusted life years for chronic respiratory diseases from 1990 to 2017: systematic analysis for the Global Burden of Disease Study 2017.” bmj 368 (2020).

Articolul Smoking during the pandemic, ping-pong between panic and stupidity apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

But official reports published by clinicians fighting Covid-19 state that disordered blood clotting is present in most infected patients severely affected. (1)

In the case of Coronavirus infection, we do not know if this disordered coagulation increases the risk of severe disease, or if the virus increases the risk of disordered coagulation. But what we do know from the influenza virus infection is that it helps the virus become more aggressive, amplifying viral replication. (2)

Of course, we also know that pre-existent cardiovascular disease increases the risk of severe infection, that the infection in itself can associate cardiovascular complications, and that the treatment of the infection can cause cardiovascular side effects. (3)

However, this disordered coagulation occurs, indicating a severe prognosis in patients infected with Coronavirus. (4)

But many people with multiple comorbidities including pre-existing cardiovascular disease and many of the elderly take anticoagulant medication. And many dietary supplements and herbal remedies interact with this anticoagulant medication.

Dietary supplements with vitamins E and K, omega-3 fatty acids, selenium, coenzyme Q-10 or arginine impacts blood clotting. (5,6)

Vitamin D supplements can act as a double-edged sword when it comes to their cardiovascular effect, studies showing that both hypovitaminosis through insufficient dietary intake and hypervitaminosis by taking vitamin D supplements when you are not deficient can have a harmful cardiovascular impact. (7) And the current scientific evidence shows that vitamin D supplements protects against respiratory infections only those with vitamin D deficiency. (8)

Related to vitamin C supplements, the current scientific evidence contradicts both the harmful impact of vitamin C supplements on blood coagulation and the effectiveness of vitamin C supplements in preventing respiratory infections.

• The harmful impact on blood coagulation is assumed based on individual case reports not on objective evidence. (9, 10)
• The only people for whom there is evidence of minimal efficiency in the prevention of colds are athletes and soldiers, but also in their case the therapeutic dose is 200 mg per day, five times less than the gram taken by the majority of people trying to increase their immunity. (11)

There are numerous herbal remedies that can associate coagulation disorders, increasing the risk of thrombosis or bleeding in people on anticoagulant treatment, including: aloe, echinacea, ginseng, ginger, chamomile and alfalfa. (12,13)

Obviously, there is no need to worry about drinking a chamomile tea in the morning. But the safety of using herbal remedies containing concentrated extracts of such plants is not proven in patients under anticoagulant treatment. (14)

There are also foods that in the case of excessive consumption can influence blood coagulation, such as: cranberries, garlic, spinach, arugula, green salad, valerian, nettles, asparagus, cauliflower, cabbage and broccoli. However, scientific evidence shows that patients under anticoagulant treatment should only consume these moderately, not exclude them. (15)

On the other hand, during the current period it would be prudent to avoid the use of dietary supplements and herbal remedies that can interfere with blood clotting because – as opposed to these foods that should not be excluded – dietary supplements and herbal remedies have a much higher content of active substances.

A higher concentration of active substances does not mean a better impact, but a stronger impact. And – although most believe that dietary supplements and herbal remedies do not have side effects because they are natural – these products can have side effects, as this stronger impact can also be negative. (16)

As I wrote in the article about Coronavirus, immunity is a much more complex system than it seems when talking about immunity while having a Corona.

The link between immunity and nutrition is a complicated tango, (17) optimizing immunity requiring long term healthy eating, (18) high quality sleep, (19) and the life-long practice of physical exercise. (20)

Dietary supplements and herbal remedies are not without side effects because they are natural. (21)

Their side effects are less acknowledged because they are less evaluated in comparison to medicines, being produced and marketed according to legal regulations different from those for medicines, regulations that do not require rigorous testing in the elderly or in people with multiple comorbidities – that is, exactly those who are at higher risk today. (22)

What healthy people risk when taking all kinds of supplements to increase immunity is liver toxicity. (23)

What the elderly and people with multiple comorbidities under anticoagulant treatment risk when taking all kinds of supplements to increase immunity alongside their medication is liver toxicity and disordered coagulation. (24)

Because abnormal blood clotting is one of the red flags indicating severe prognosis in people infected with Coronavirus, at least until the current state of things comes to peace, it is more prudent to optimize immunity through healthy eating, proper sleep and physical exercise.

References

(1) Tang, Ning, et al. “Abnormal Coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia.” Journal of Thrombosis and Haemostasis (2020).

(2) Yang, Yan, and Hong Tang. “Aberrant coagulation causes a hyper-inflammatory response in severe influenza pneumonia.” Cellular & molecular immunology 13.4 (2016): 432-442.

(3) Driggin, Elissa, et al. “Cardiovascular Considerations for Patients, Health Care Workers, and Health Systems During the Coronavirus Disease 2019 (COVID-19) Pandemic.” Journal of the American College of Cardiology (2020).

(4) Han, H., et al. “Prominent changes in blood coagulation of patients with SARS-CoV-2 infection.” Clinical chemistry and laboratory medicine (2020).

(5) Shea, M. Kyla, and Sarah L. Booth. “Vitamin E: Interactions with Vitamin K and Other Bioactive Compounds.” Vitamin E in Human Health. Humana Press, Cham, 2019. 261-269.

(6) Stanger, Michael J., et al. “Anticoagulant activity of select dietary supplements.” Nutrition reviews 70.2 (2012): 107-117.

(7) Zechner, Christoph, and Dwight A. Towler. “Vitamin D: Cardiovascular Effects and Vascular Calcification.” Vitamin D. Academic Press, 2018. 549-570.

(8) Martineau, Adrian R., et al. “Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data.” bmj 356 (2017): i6583.

(9) Feetam, Celia L., R. H. Leach, and M. J. Meynell. “Lack of a clinically important interaction between warfarin and ascorbic acid.” Toxicology and applied pharmacology 31.3 (1975): 544-547.

(10) Sattar, Adil, Jane E. Willman, and Raghu Kolluri. “Possible warfarin resistance due to interaction with ascorbic acid: case report and literature review.” American journal of health-system pharmacy 70.9 (2013): 782-786.

(11) Hemilä, Harri, and Elizabeth Chalker. “Vitamin C for preventing and treating the common cold.” Cochrane Database of Systematic Reviews 1 (2013).

(12) Ulbricht, C., et al. “Clinical evidence of herb-drug interactions: a systematic review by the natural standard research collaboration.” Current drug metabolism 9.10 (2008): 1063-1120.

(13) Cho, William CS. “Herb-drug interactions: systematic review, mechanisms, and therapies.” (2015).

(14) Cordier, Werner, and Vanessa Steenkamp. “Herbal remedies affecting coagulation: a review.” Pharmaceutical biology 50.4 (2012): 443-452.

(15) Violi, Francesco, et al. “Interaction between dietary vitamin K intake and anticoagulation by vitamin K antagonists: is it really true?: a systematic review.” Medicine 95.10 (2016).

(16) Posadzki, Paul, Leala K. Watson, and Edzard Ernst. “Adverse effects of herbal medicines: an overview of systematic reviews.” Clinical medicine 13.1 (2013): 7.

(17) Venter, Carina, et al. “Nutrition and the Immune System: A Complicated Tango.” Nutrients 12.3 (2020): 818.

(18) Goldsmith, Jason R., and R. Balfour Sartor. “The role of diet on intestinal microbiota metabolism: downstream impacts on host immune function and health, and therapeutic implications.” Journal of gastroenterology 49.5 (2014): 785-798.

(19) Faraut, Brice, et al. “Immune, inflammatory and cardiovascular consequences of sleep restriction and recovery.” Sleep medicine reviews 16.2 (2012): 137-149.

(20) Jang, Tae-Yeong, and Bong-Woo Chang. “Meta-analysis of the Influence of then Elderly Regular Exercise on their Immunity.” Journal of Digital Convergence 15.5 (2017): 339-344.

(21) Stickel, Felix, and Daniel Shouval. “Hepatotoxicity of herbal and dietary supplements: an update.” Archives of toxicology 89.6 (2015): 851-865.

(22) Navarro, Victor J., and M. Isabel Lucena. “Hepatotoxicity induced by herbal and dietary supplements.” Seminars in liver disease. Vol. 34. No. 02. Thieme Medical Publishers, 2014.

(23) García-Cortés, Miren, et al. “Hepatotoxicity by dietary supplements: a tabular listing and clinical characteristics.” International journal of molecular sciences 17.4 (2016): 537.

(24) Gardiner, Paula, Russell S. Phillips, and Allen F. Shaughnessy. “Herbal and dietary supplement-drug interactions in patients with chronic illnesses.” American family physician 77.1 (2008): 73-78.

Articolul Dietary supplements affecting blood clotting apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

On December 30, 2019, in a small fish and meat market where 1500 worked, in a crowded Chinese city with 11 million inhabitants, some workers got sick. And because they felt quite sick, each decided to go see a doctor in the hope that they still could somehow spend the New Year’s Eve in the family. And this is how the Wuhan on-call doctors got to see these patients suffering from a type of pneumonia that was not very responsive to traditional treatments. (1)

They scratched their heads for days and nights and tried their best to deal with the weird flu until – January 7, 2020 – when dr. Shi Zhengli’s team, a local virologist, informed them that the strange disease is a zoonosis caused by a virus from the Coronavirus family which normally affects bats.

We do not know if the pandemic declared on Wednesday by the World Health Organisation (WHO) broke out because the use of soap is one of the behaviours that distinguish people from animals or because some people have started to eat vampire bats. However, as direct descendants of father Dracula, we should take the stories of humans eating vampires at least with a grain of salty garlic.

Because the panic and the brain work in shifts, Coronavirus managed to divide the planet in two:

1. either you are scared – and you just realised that soap was invented
2. either you are rational – and you look in dismay at how seemingly mentally healthy people started to queue up to buy soap

Well… there is also the third category: the careless people continuing to live their lives like nothing happens on the planet.

This article is not a call to carelessness, it is a call to reason.

Because panic amplifies irrational behaviours whose consequences can unbalance us all, it is important to see the situation as it is: neither better, nor worse than it is.

The problem is complicated not only by the fact that fear freezes the brain, but also by the fact that the very brain humans operate on comes with at least one factory defect:

The more we read and hear about a thing that rarely happens the more we expect it to happen despite knowing deep in our minds that it rarely happens – which is called  “availability bias“. (2)

The more we hear about Coronavirus, the more it looks like it sits and looks at us through the kitchen window like a vampire – ready to jump and grab us by the shoulders to suck out our lungs.

Researchers warned us for years and years that the way pandemic infectious diseases are communicated and managed has a major financial impact, the perception of risk having a more harmful impact than the disease itself. (3)

In the rare times when we would still decide to use our neocortex, we could look at Chinese officials report which shows that:

• 81% of infected people had only mild respiratory symptoms if at all, more than half presenting without having a fever
• 14% of infected people developed severe respiratory disease, needing Intensive Care
• and the 5% of the infected people that developed severe respiratory disease who put their lives at risk were sick and old, most very sick and very old (4)

Despite official reports showing that most people who get infected only develop mild respiratory disease, on Wednesday – March 11, 2020, WHO declared the current global situation a pandemic because the number of cases reached 118,000 worldwide, of which 4,291 have died.

Risk perception doubled since pandemic has been declared in spite of the fact that even in Italy – the most affected country besides China – official reports show that 91% of infected people have only mild disease.

The majority of people do not understand what a pandemic actually means, although the flu regularly reaches pandemic levels and although most – even those very ill or exposed – usually ignore it and refuse to get vaccinated.

But what we know from the former pandemics we went through is that the most harmful impact is generated by people’s perception of risk, affecting mainly the economy of the countries not the health of the people.

Pandemic does not mean that the disease has changed or that it became more aggressive.

Pandemic means that many people are affected worldwide.

It shows the disease is highly contagious, not highly aggressive.

– How many of us haven’t had a cough or a fever this winter?

According to the report published by WHO on March 12, Coronavirus mortality is 3.6% – a simplistic figure obtained by dividing the number of deaths by the number of officially known cases.

And this simplistic figure built on the known cases is the root of all mathematical speculations that feed people’s panic. But it’s a fake number.

Although the 3.6% mortality rate looks enormous when compared to the minuscule 0.1% mortality rate of the flu, most experts remain quite calm stating that if you compare apples with pears lice come out when the aliens no longer land in Antarctica because Tuesday is blue.

Most infectious disease experts remain calm because of the 118.000 people officially infected with Coronavirus those who got severely affected were either very old or already very sick before catching up the virus, having multiple other diseases besides the last drop of corona.

And most mathematics experts remain calm because without proper testing the powerful stage effect – obtained by the fervent media coverage of the shiny 3.6% COVID-19 mortality as “huge” when compared with the 0.1% flu mortality – cannot wipe out the only two things we actually know despite the global madness:

1. of 100 people infected with Coronavirus 96,4 survive 
2. the 3.6% mortality figure is a fake number because it is based on the number of officially known cases not on the actual number of cases

Just that not all mathematicians remain calm, some mathematicians making statistical estimates based – maybe – on accepting the fact that in general the masses of panicked people behave irrationally, and individually many people do not care enough about other people to respect minimum common sense recommendations.

It seems that common sense is not that common.

Besides the low incidence of common sense, the mathematicians who don’t remain calm quote the exponential growth bias – another bias that usually affects human’s thinking. According to this thinking flaw, most people do not understand that a small problem can grow exponentially, so they ignore it. (5)

But the mathematicians that remain calm in this global madness state that Coronavirus pandemics doesn’t present exponential growth and that the prediction models built on exponential growth mathematical models can be misused in pandemics. (6)

So, today we witness a world of panic inflated by assumptions psychologically complicated by the media spot light on the horror stories that try to justify the global problem built mathematically on predictions over which even mathematicians don’t agree upon.

Because of insufficient testing:

• and, because the majority of infected people don’t even have a fever, we cannot know that the known number of cases is the number of cases
• and, because the mortality figure is obtained by dividing the number of deaths to the number of known cases, the mortality figure would be very different if we would know the actual number of cases
• and, because of the induced panic, the mathematically built worldwide problem will end up costing us all financially as the economy will take the actual fall (7)

Based on the fact that current statistics confirm the initial Chinese report proving that more than 80% of the people who get infected with Coronavirus have no or only mild symptoms – purely mathematically – the total number of worldwide cases could be 5 times higher than the officially known number.

And this would mean nothing bad if we’d had the discipline and the responsibility to respect the minimum recommended prevention.

What we know is that the risk of getting the disease is high, not that the risk of mortality from this disease is high.

A higher number of cases does not mean that the disease is more aggressive.

A higher number of cases means the disease is more contagious.

More contagious does not mean more aggressive.

Aggressivity is about the probability of dying from the disease not about just getting the disease.

COVID-19 is contagious. SARS was aggressive.

Theoretically, we are required to do the least possible: to stay in the house when we have respiratory symptoms or when we know that we’ve just traveled back from areas affected by the virus, not to kiss the elderly and to wash our hands. But for common sense recommendations to be effective you have to have common sense. And because many do not have common sense, prolonging the application of these initially minimum recommendations, cumulatively will end up highly expensive for all.

Each pandemic is different depending on:

• disease factors: how contagious it is and how aggressive it is
• human factors: like the age and state of health or hygiene
• health system factors: such as adequate access to protective equipment, the capacity of intensive care units and the fact that physicians and other unprotected medical personnel can become the first line of victims of others’ panic and lack of common sense
• science factors: how fast researchers can come up with:
  • diagnostic kits able to accurately identify affected individuals
  • effective treatments for the current outbreak
  • vaccines to prevent future ones

If the disease induced by the Coronavirus infection is more contagious but 80% of the infected people just cough, most without even having a fever, then the global number of cases could be 590.000, and mortality 0.7%.

And yes, 0.7 is still 7 times higher than the 0.1 flu mortality, but this does not erase the fact that from 100 Coronavirus-infected people 99.3 will be ok.

But you cannot say anymore that 99.3 of 100 infected people will be ok after the economic consequences of the assumptions you officially trumpeted began to emerge, exactly as you patchily did in 2003 with the far more aggressive SARS. (8)

Aligned with the many thinking biases described by Tversky and Kahneman in the 1970s, once they take an official stance most people tend to continue to defend it even when their own evidence contradicts them. And those managing the COVID-19 pandemic are people too. So the global madness will continue based on the only factor they can pin down: the high contagiousnessț impact on the exponential growth.

But the evolution of the disease does not show exponential growth.

When the reality of the disease contradicts you but the economic consequences of the wrong statistic presumptions you made have begun to appear, you cling to any evidence that might justify what you assumed:

• the population at higher risk
• and the fall of the medical system

To protect yourself from the economic consequences of the panic created globally, of the 100 infected that mostly have nothing you fervently put the spot light on the only 1 that’s doing worse and hope that no one with sufficient economic and political power will grab you by the collar to ask why the hell do you put the spot light on this 1 when 99.3 are fine.

Just that treating the population at higher risk and the resources required for the medical system to keep working cost money and all systems risk to fall including the medical system when there will be no money because we neglected economy while trying to preserve health.

The disease induced by Coronavirus is mainly mild.

Without proper testing, mortality seems higher than influenza’s but officially available mortality figures don’t indicate an exponential growth.

People that were already damaged by advance age or advanced disease before Coronavirus will be more affected.

Health care systems that were already damaged before the Coronavirus will be more affected.

Officially, WHO recommends:

• to greet each other at least one meter distance
• to cough in the elbow
• to stay home if we feel ill
• to wash our hands
• and to clean up our homes and spaces

Officially, WHO doesn’t even recommend to wear a mask without first having cough or a fever, specialists recommending them only to those having symptoms and to those taking care of them because:

• most masks available on the market are not appropriate
• most people who have access to appropriate masks do not use them properly
• and because the actual number of masks and other protective medical devices available on the planet is limited, even the medical personnel risking to remain without them due to the panic created in the general population

However, in spite of the fact that unlike the flu Coronavirus doesn’t seem to severely affect children and teenagers and in spite of the available analyses of past pandemics showing that school closure has tripled economic harm in countries such as England, France, Belgium and the Netherlands (9), the UNICEF and WHO stands is the quoted reason behind the closure of schools.

– Who cares that school closure and the absenteeism generated by panic worsens the economic impact? (10)

Ignoring the fact that everyone’s access to any medical treatment decreases if our financial capacity drops down to caves levels, we close schools to protect the 3.6 grandparents out of those 100 grandparents over the age of 80 or with more illnesses than they can carry assuming they might get infected by their grandchildren who’d go to school.

And while schools are deserted to protect the vulnerable grandparents, the parks are full with vulnerable grandparents taking their grandchildren out to have some fun like in a global unplanned holiday.

The disease is mild and the spread might end if 76% of transmissions would stop. (11) But adding to the fact that the vulnerable population seems to mock our efforts to protect them, some of the people officially diagnosed as being infected with Coronavirus do not respect the fact that by leaving the house others will be infected.

Just like for years, as a mother, I had to deal with the consequences of other parents bringing their sick children to school despite the risk of infecting other children – of a mild flu – now we witness in dismay how people at risk and people officially infected or people who traveled back from high risk areas of the globe just casually go outside, enjoying the spring warm weather.

We respectfully stay home to protect the vulnerable population, while the vulnerable population casually goes out to the beach, having barbecues, meeting their friends at the mall then panically buying everything that falls into their hands, sitting at endless queues for food and soap.

We stay home although we could work.

Old people and those diagnosed with or at risk of a coronavirus infection are walking the streets spending their last dime on beans, vitamins and soap resting assured that the Easter Bunny and Santa Claus will take care of them when they will eventually run out of money.

– What are you going to eat a month from now if you spend all your money today on perishables?

– Face masks and soap?

Reading official reports, during the past few weeks I wondered if we globally went batshit crazy …

Not that I complain of the light traffic in Bucharest or of the joy of my children generated by the unplanned holiday that gradually translated to boredom. But Coronavirus has filled my Inbox with two types of emails:

1. some making the same demand: “What should I buy to increase my immunity?“
2. and some making the same offer: “What can we sell you to increase your immunity?“

Like at the market: demand and supply.

And if the answer to the second question is a simple SPAM report thinking “the mother of the idiots is always pregnant“, the answer to the first question seems somewhat more complicated because the vast majority of people think this is THE time when you have to take something to increase your damn immunity.

Obviously, the vast majority of people does not want to address the fact that eating fast food and drinking soda drinks on the run (12) during stressful days followed by nights with low quality, insufficient sleep (13) decreases immunity.

The vast majority of people has no idea what “immunity” is, the subliminal message passed on from one good doer to another being that you have to take vitamins, antioxidants or something.

Most believe that “immunity” is bought at the pharmacy.

Just that only “immunity” is bought at the pharmacy.

Immunity without quotation marks depends on the healthy eating (14), on the regular life-long practice of sports (15, 16), on the high quality sleep (17), and even on the well-being and overall happiness level of your life (18). So yes, it seems damn tricky to increase immunity so suddenly now with this Coronavirus sneaked out of the dark Chinese vampires’ caves in the fast food-sedentary-stressful-unhappy life.

Just that, although we are encouraged to take all sorts of stuff to somehow defend ourselves against this dark virus, the only two things you can actually do to increase your immunity specifically against Coronavirus are:

1. to get infected with Coronavirus
2. to get vaccinated with a vaccine specifically created against this virus

We have no vaccine yet.

And exactly as everybody wants to go to heaven, but nobody wants to die, there isn’t anybody who’d want to get infected.

Without getting sick and without the vaccine, the only thing you can increase by taking all sorts of vitamins, plants and miracle natural remedies is is the non-specific part of the immune system, the innate immunity.

But increased non-specific immunity does not specifically defend you against Coronavirus or against anything else for that matter.

Non-specific immunity is called “non-specific” because it is non-specific.

And increasing non-specific immunity does not mean improved health.

Increased non-specific immunity means deregulated immune system, bone and gastrointestinal inflammatory disease, allergies, autoimmunity. (19)

And it is absolutely pointless to take any magic plant or vitamin for the purpose of increasing non-specific immunity.

Non-specific immunity is directly increased by stress, sedentariness, insufficient sleep and by the very western diet by their pro-inflammatory effects. (20)

Immunity without quotation marks is a much more complex system than it seems when talking about immunity while having a Corona.

The upside of the Coronavirus story is that it has managed to increase interest in seemingly uninteresting products. Like soap.

The downside is that if this global panic continues, we will not die of Coronavirus but of poverty.

It all started at the market and it will all end at the market.

I’m not sure if it’s like at the small fish and meat market in Wuhan where some of the 1500 workers got infected, but all this seems kind of an expensive trade that ignores the fact that in order to have something to sell someone still has to actually work.

References

(1) Phelan, Alexandra L., Rebecca Katz, and Lawrence O. Gostin. “The novel coronavirus originating in Wuhan, China: challenges for global health governance.” Jama 323.8 (2020): 709-710.

(1) Phelan, Alexandra L., Rebecca Katz, and Lawrence O. Gostin. “The novel coronavirus originating in Wuhan, China: challenges for global health governance.” Jama 323.8 (2020): 709-710.

(2) Tversky, Amos, and Daniel Kahneman. “Availability: A heuristic for judging frequency and probability.” Cognitive psychology 5.2 (1973): 207-232.

(3) Smith, Richard D. “Responding to global infectious disease outbreaks: lessons from SARS on the role of risk perception, communication and management.” Social science & medicine 63.12 (2006): 3113-3123.

(4) Wu, Zunyou, and Jennifer M. McGoogan. “Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: summary of a report of 72 314 cases from the Chinese Center for Disease Control and Prevention.” Jama (2020).

(5) Levy, Matthew R., and Joshua Tasoff. “Exponential-growth bias and overconfidence.” Journal of Economic Psychology 58 (2017): 1-14.

(6)Chowell, Gerardo, and Cécile Viboud. “Is it growing exponentially fast?–impact of assuming exponential growth for characterizing and forecasting epidemics with initial near-exponential growth dynamics.” Infectious disease modelling 1.1 (2016): 71-78.

(7) Ayittey, Foster Kofi, et al. “Economic impacts of Wuhan 2019‐nCoV on China and the world.” Journal of Medical Virology (2020).

(8) Lee, Jong-Wha, and Warwick J. McKibbin. “Globalization and disease: The case of SARS.” Asian Economic Papers 3.1 (2004): 113-131.

(9) Keogh-Brown, Marcus Richard, et al. “The macroeconomic impact of pandemic influenza: estimates from models of the United Kingdom, France, Belgium and The Netherlands.” The European Journal of Health Economics 11.6 (2010): 543-554.

(10) Smith, Richard D., Marcus R. Keogh-Brown, and Tony Barnett. “Estimating the economic impact of pandemic influenza: an application of the computable general equilibrium model to the UK.” Social science & medicine 73.2 (2011): 235-244.

(11) Read, Jonathan M., et al. “Novel coronavirus 2019-nCoV: early estimation of epidemiological parameters and epidemic predictions.” medRxiv (2020).

(12) Tall, Alan R., and Laurent Yvan-Charvet. “Cholesterol, inflammation and innate immunity.” Nature Reviews Immunology 15.2 (2015): 104-116.

(13) Prather, Aric A. “Sleep, stress, and immunity.” Sleep and Health. Academic Press, 2019. 319-330.

(14) Childs, Caroline E., Philip C. Calder, and Elizabeth A. Miles. “Diet and Immune Function.” (2019): 1933.

(15) Duggal, Niharika A., et al. “Can physical activity ameliorate immunosenescence and thereby reduce age-related multi-morbidity?.” Nature Reviews Immunology 19.9 (2019): 563-572.

(16) Jang, Tae-Yeong, and Bong-Woo Chang. “Meta-analysis of the Influence of then Elderly Regular Exercise on their Immunity.” Journal of Digital Convergence 15.5 (2017): 339-344.

(17) Ganz, Freda DeKeyser. “Sleep and immune function.” Critical care nurse 32.2 (2012): e19-e25.

(18) Ayling, Kieran, Kanchan Sunger, and Kavita Vedhara. “Effects of brief mood-improving interventions on immunity: a systematic review and meta-analysis.” Psychosomatic medicine 82.1 (2020): 10-28.

(19) Statovci, Donjete, et al. “The impact of western diet and nutrients on the microbiota and immune response at mucosal interfaces.” Frontiers in immunology 8 (2017): 838.

(20) Poutahidis, Theofilos, et al. “Microbial reprogramming inhibits Western diet-associated obesity.” PloS one 8.7 (2013): e68596.

Articolul Coronavirus – batshit crazy spring rolled Devil’s baby apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

The image of a universal panacea is increasingly promoted by both health workers and patients contributes to the fact that in 2019 the sale of vitamin D supplements registered a profit of $ 1.1 billion, players in the dietary supplement market expecting this profit to reach $ 1.7 billion in 2025.

And it is “waiting” not “estimating” because in market reports such as“Vitamin D market”, those who might be interested are trained how to educate people to buy more and more.

It’s just that vitamin D is not a magical supplement that wipes away any disease, it is a physiologically active hormone that can spell nothing but side effects when taken without a proven vitamin D deficiency as a leaf in the wind of the pharmaceutical industry.

Sadly, being a dietary supplement, you can be be educated indirectly by the same supplement manufacturers to blame any side effects they might cause on anything and everything else besides them, as these manufacturers are not required by law to demonstrate either that these supplements do what they say they do, nor that these supplements do not have side effects.

When you buy and use dietary supplements you are a “client” not a “patient”, regardless of whether the person who prescribed them to you is a physician or not. Physicians do not have the professional training to prescribe dietary supplements. Nobody has the professional training to prescribe dietary supplements. Dietary supplements are promoted not “prescribed” because dietary supplements are legally defined as “foods” not as “drugs”.

In todays’s hectic life, the hope that you could prevent something, anything, by simply taking a pill instead of the healthy lifestyle you know you should actually have is ever more present – although even on these products’ label is written black on white that they cannot replace a healthy lifestyle.

– Who cares if maybe they cannot?

– Maybe they can.

– Just that the current scientific evidence shows that they mainly cannot.

The efficiency of using vitamin D supplements for the prevention of various diseases ranging from cancer to cardiovascular disease is an assumption unsupported scientific evidence. (1, 2, 3)

Hypovitaminosis D is one of the many consequences of an unhealthy lifestyle, not the cause of illnesses that result from the unhealthy lifestyle you keep trying to hide by taking supplements.

Both hypovitaminosis D and these illnesses are consequences. The cause of these illnesses is the unhealthy lifestyle not the lack of vitamin D. And the cause does not disappear when if you somehow manage to wipe away one of the consequences. Even vitamin D deficiency doesn’t disappear when you take vitamin D supplements if you don’t have the deficiency first.

And, if scientific evidence points to the fact that preventing various diseases by using vitamin D supplements is just a cozy assumption, current scientific evidence shows that the efficacy of using vitamin D supplements to prevent osteoporosis in the absence of vitamin D deficiency is another cozy assumption. (4)

A physician recommending dietary supplements is not practicing medicine, he practice marketing. As cozy, inefficient and unprofessional as when a beautician would recommend artificial tanning devices to achieve an appropriate vitamin D status. (5) And of course we can mock science by inviting evidence based medicine fans to participate in a double blind, randomised, placebo controlled, crossover trial of the parachute. (6)

Regardless of the core profession, dietary supplement promoters are taught how to educate you to feel that you need these products by the pharmaceutical industry, not by independent labs or objective researchers who scientifically prove that vitamin D supplementation of any good to those without a vitamin D deficiency.

Despite the fact that today being popular seems more important than being physiologically correct, vitamin D supplements show no efficacy without deficiency, (7, 8) and osteoporosis prevention is far more complicated than taking some pill.

References

(1) Beveridge, Louise A., et al. “Effect of vitamin D supplementation on markers of vascular function: a systematic review and individual participant meta‐analysis.” Journal of the American Heart Association 7.11 (2018): e008273.

(2) Autier, Philippe, et al. “Effect of vitamin D supplementation on non-skeletal disorders: a systematic review of meta-analyses and randomised trials.” The lancet Diabetes & endocrinology 5.12 (2017): 986-1004.

(3) Manson, JoAnn E., et al. “Vitamin D supplements and prevention of cancer and cardiovascular disease.” New England Journal of Medicine 380.1 (2019): 33-44.

(4) Reid, Ian R., Mark J. Bolland, and Andrew Grey. “Effects of vitamin D supplements on bone mineral density: a systematic review and meta-analysis.” The Lancet 383.9912 (2014): 146-155.

(6) Pierret, Lauranne, et al. “Overview on vitamin D and sunbed use.” Journal of the European Academy of Dermatology and Venereology 33 (2019): 28-33.

(6) Smith, Gordon CS, and Jill P. Pell. “Parachute use to prevent death and major trauma related to gravitational challenge: systematic review of randomised controlled trials.” Bmj 327.7429 (2003): 1459-1461.

(7) Fassio, A., M. Rossini, and D. Gatti. “Vitamin D: no efficacy without deficiency. What’s new?.” Reumatismo 71.2 (2019): 57-61.

(8) Reid, Ian R., and Mark J. Bolland. “Controversies in medicine: the role of calcium and vitamin D supplements in adults.” Medical Journal of Australia (2019).

Articolul Vitamin D supplements – hype and physiology apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Although the decrease in LDL-cholesterol has been Our Holly Father in preventive cardiology for decades, LDL-cholesterol lowering drugs only lower LDL-cholesterol. And that’s all. Nothing more. Nothing less.

If you scratch your brain asking yourself “- What: “And that’s all”?!“ means, it is important to note that lowering LDL-cholesterol does not help most people prevent anything:

• in the case of statins, the absolute clinical benefit is 10% = 90 out of 100 people take the medicine for nothing, paying an average of 20 euros per month only for potential side effects (Collins et al., 2016).
• in the case of evolocumab, the absolute clinical benefit is only 1.5% more than statins = 65 out of 66 people take the medicine for nothing, paying 1,000 euros per month only for potential side effects (Sabatine et al., 2017).

44 randomized controlled trials indicate that lowered LDL-cholesterol does not associate with lowered mortality (DuBroff, 2017), the difference in survival between people with high cardiovascular risk who take statins compared to those who do not take statins being only 4 days (Kristensen, Christensen and Hallas, 2015).

In addition to these findings, some tend to forget or ignore the randomized controlled trial published in 2007 in the New England Jornal of Medicine, a study of 15,067 people at high cardiovascular risk. This study was stopped in progress despite the fact that the drug tested was very effective, combining a 72.1% increase in HDL-cholesterol and a 24.9% decrease in LDL-cholesterol. Only that, despite the improvement of the lipid profile, the actual clinical outcome was increased mortality (Barter et al., 2007).

The hope that lowering LDL-cholesterol lowers cardiovascular mortality is contradicted by the current scientific evidence – evidence that you can read by clicking on the cited links. However, hope dies last, in the meantime helping:

1. the researcher in search of sponsors – to be satisfied that he contributes to saving humanity from death by cardiovascular diseases – the purpose being to discover new drugs to lower cholesterol, not to improve patient’s health
2. the physician that prescribes statins on autopilot without consulting his own brain – to be satisfied that he has recommended something to the patient – the purpose being to write the prescription, not to improve the patient’s health
3. the pharmacist looking for paying customers – to be satisfied that he made his sales plan today – the purpose being to sell drugs, not to improve the patient’s health
4. the patient with no willingness to invest nothing but money in his own health – to be satisfied that he kind of contributes to his own health by buying from the pharmacist the prescription recommended by the doctor based on the studies carried out by the researcher – the purpose being to take the pill or the injection administration, not to improve the patient’s condition because he does not identify with the status of “patient”. He is George, Maria or Costel – the person, not “the patient” – and he did everything he was told to do: he went to the doctor, he received a prescription, he took the pills. End of story.

Cardiovascular disease prevention by statins alone works as efficiently as the lovely story of the four people: Everybody, Somebody, Anybody and Nobody:

“There was an important job to be done and Everybody was sure that Somebody would do it. Anybody could have done it, but Nobody did it. And it all ended up with Everybody blaming Somebody when Nobody did what Anybody could have done.”

Everyone is satisfied: we manage to lower LDL-cholesterol. The LDL lowering box is ticked, we’re all good. At least on paper (Diamond and Ravnskov, 2015).

Only that the satisfaction of all these people including George, Maria and Costel cost the health and quality of life of the “patient George, Maria or Costel”, without bringing them any clinical benefit other than the lowering of “bad-bad-bad” LDL-cholesterol (de Lorgeril and Rabaeus, 2015).

Improved blood tests, dead patient. The funeral dinner party and the LDL-cholesterol lowering success congratulations later – each according to the available possibilities. Common menu: burger with fried potatos and a sugar-free cola (to reduce calories) bought on the run from the local Drive Through, eaten also on the run and finished triumphantly with throwing on the window of smoking stumps while driving to the job you hate but have to go to every damn day to pay your bills,  lovely place on Earth where you would elegantly sing the entire repertoire of Paraziții (n.a. a Romanian hip-hop group, with dirty language and virulent lyrics).

Cardiovascular risk is multifactorial, lowering LDL is just a single unknown factor in an equation with many other ultra-cognitive things that we DON’T want to, CAN’T, DON’T have time for, DON’T find it EASY to, DON’T feel COMFORTABLE the need to – DON’T LIKE to address them today:

• sedentary normoponderal persons have a higher cardiovascular risk than overweight individuals who regularly practice sports (Pandey, Berry and Lavie, 2015; Mainous III et al., 2019)
• smoking increases cardiovascular risk, but the risk gradually decreases after smoking cessation (Aune et al., 2018; 2019)
• hookah smoking (water pipe smoking) increases cardiovascular risk (Bhatnagar et al., 2019)
• electronic cigarette smoking contributes to increased cardiovascular risk both through the intake of toxic substances and by decreasing the chances of actually ever quitting smoking (Glantz and Bareham, 2018)
• insomnia increases cardiovascular risk (Sofi et al., 2014; Fernandez-Mendoza, 2019)
• depression and anxiety increase cardiovascular risk (Wulsin and Singal, 2003; Suls et al., 2018), completely ignoring the fact that people diagnosed with familial hypercholesterolemia have a higher level of depression and anxiety (Akioyamen et al., 2018). Fortunately, however, psychotherapy can contribute to lower cardiovascular mortality in people with high cardiovascular risk (Richards et al., 2018).
• metabolic syndrome increases cardiovascular risk (Mottillo et al., 2010)
• liver steatosis increases cardiovascular risk (Targher, Day and Bonora, 2010)
• obesity increases cardiovascular risk (Eckel et al., 2016)
• in the case of normal-weight persons with high cardiovascular risk, excess fat stored on the abdomen increases the cardiovascular risk (Coutinho et al., 2011)
• weight loss for the sake of weight loss through brain-dead but popular diets leads to long-term metabolism disorders and increases cardiovascular risk (Chaston and Dixon, 2008; Lavie et al., 2016)
• people who are too slim, with too little fat, also have an increased cardiovascular risk (Chehab, 2008)

We will address these issues on Monday. Next Monday. Or the next.

Sedentarism, smoking, insomnia, depression, anxiety, metabolic syndrome, hepatic steatosis, abdominal fat storage, underweight or obesity of the patient George, Maria or Costel are frequently ignored by both George, Maria or Costel, as well as most autopilot-recipes-writers calling themselves physicians (Daniels, Pratt and Hayman, 2011; Vancheri et al., 2016).

And I highlight the automatism of the autopilot-recipes-writers because the international medical community is divided: some doctors consider statins a damn crap, while others consider statins the golden egg that will save anyone over the age of 50 (Rabaeus et al., 2017; McCartney, 2012).

The patient with primary or secondary cardiovascular risk who is taking their medication + properly improves their nutrition + gives up smoking + works on assertiveness (and possibly practice some for of meditation instead of swallowing his frustration while passive-agressivingly cursing his boss or his wife in his mind) and who also practices regular sports = gets LDL-cholesterol lowering + cardiovascular risk lowering ± side effects. All three consequences of disciplined and improved eating beahavior and life style but only as long as he administers his medication and practices his healthy lifestyle and nutrition.

The patient who only takes her 20 euro pills or who only administers his 1,000 euro injection but who does not improve his quality of life and nutrition = only gets LDL-cholesterol lowering ± side effects. Both only as long as he administers his medication.

The lowering of the LDL-cholesterol trumpeted out loud by different eminences at various congresses and conferences – where we charm the audience with relative values, while hiding absolute values – is the way in which statins are pushed forward in the working mind of the autopilot-recipes written by those doctors who do not bother with improving patient’s health. Especially if the patient does not bother himself with improving patient’s health. Why would the doctor care more about the patient than the patient cares about the patient?

The patient wants a quick fix. You got it!

Decreasing LDL-cholesterol helps the researcher to have something to present at the congresses, it helps the doctor to have what to recommend and it helps the pharmacist to have what to sell. Only that without sports, without giving up smoking, without fat loss (not water and muscles loss), without developing mental strategies to counteract stress conditions, and without assuming responsibility by George, Maria and Costel it has zero benefits for the patient. And the even harder part is that to work, these behaviors must be practiced daily FOR THE ENTIRE DAMN LIFE.

Cardiovascular mortality is increasing worldwide because most aren’t practicing the healthy eating and lifestyle behaviors.

But although it sounds like the hard work no one is actually willing to do, in the actual world we all live into not practicing these behaviors cannot be compensated by the administration of drugs.

Quoted studies

Akioyamen, Leo E., et al. Anxiety, depression, and health-related quality of life in heterozygous familial hypercholesterolemia: A systematic review and meta-analysis. Journal of psychosomatic research 109 (2018): 32-43.

Aune, Dagfinn, et al. Tobacco smoking and the risk of atrial fibrillation: A systematic review and meta-analysis of prospective studies. European journal of preventive cardiology 25.13 (2018): 1437-1451.

Aune, Dagfinn, et al. Tobacco smoking and the risk of heart failure: A systematic review and meta-analysis of prospective studies. European journal of preventive cardiology 26.3 (2019): 279-288.

Barter, Philip J., et al. Effects of torcetrapib in patients at high risk for coronary events. New England journal of medicine357.21 (2007): 2109-2122.

Bhatnagar, Aruni, et al. Water Pipe (Hookah) Smoking and Cardiovascular Disease Risk: A Scientific Statement From the American Heart Association. Circulation (2019): CIR-0000000000000671.

Chaston, T. B., & Dixon, J. B. (2008). Factors associated with percent change in visceral versus subcutaneous abdominal fat during weight loss: findings from a systematic review. International journal of obesity, 32(4), 619.

Chehab, F. F. (2008). Minireview: obesity and lipodystrophy—where do the circles intersect?. Endocrinology, 149(3), 925-934.

Collins, R., Reith, C., Emberson, J., Armitage, J., Baigent, C., Blackwell, L., … & Evans, S. (2016). Interpretation of the evidence for the efficacy and safety of statin therapy. The Lancet, 388(10059), 2532-2561.

Coutinho, Thais, et al. Central obesity and survival in subjects with coronary artery disease: a systematic review of the literature and collaborative analysis with individual subject data. Journal of the American College of Cardiology 57.19 (2011): 1877-1886.

Daniels, S. R., Pratt, C. A., & Hayman, L. L. (2011). Reduction of risk for cardiovascular disease in children and adolescents. Circulation, 124(15), 1673-1686.

de Lorgeril, M., & Rabaeus, M. (2015). Beyond Confusion and Controversy, Can We Evaluate the Real Efficacy and Safety of Cholesterol-Lowering with Statins?. Journal of Controversies in Biomedical Research, 1(1), 67-92.

Diamond, D. M., & Ravnskov, U. (2015). How statistical deception created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease. Expert review of clinical pharmacology, 8(2), 201-210.

DuBroff, Robert. Cholesterol paradox: A correlate does not a surrogate make. BMJ Evidence-Based Medicine 22.1 (2017): 15-19.

Eckel, Nathalie, et al. Metabolically healthy obesity and cardiovascular events: a systematic review and meta-analysis. European journal of preventive cardiology 23.9 (2016): 956-966.

Fernandez-Mendoza, J. (2019). Insomnia and cardiometabolic disease risk. In Sleep and Health (pp. 391-407). Academic Press.

Glantz, S. A., & Bareham, D. W. (2018). E-cigarettes: use, effects on smoking, risks, and policy implications. Annual review of public health, 39, 215-235.

Kristensen, M. L., Christensen, P. M., & Hallas, J. (2015). The effect of statins on average survival in randomised trials, an analysis of end point postponement. BMJ open, 5(9), e007118.

Lavie, Carl J., et al. Update on obesity and obesity paradox in heart failure. Progress in cardiovascular diseases 58.4 (2016): 393-400.

Mainous III, Arch G., et al. Effect of Sedentary Lifestyle on Cardiovascular Disease Risk Among Healthy Adults With Body Mass Indexes 18.5 to 29.9 kg/m2. The American journal of cardiology 123.5 (2019): 764-768.

McCartney, M. (2012). Statins for all?. BMJ, 345, e6044.

Mottillo, Salvatore, et al. The metabolic syndrome and cardiovascular risk: A systematic review and meta-analysis. Journal of the American College of Cardiology 56.14 (2010): 1113-1132.

Pandey, A., Berry, J. D., & Lavie, C. J. (2015). Cardiometabolic disease leading to heart failure: better fat and fit than lean and lazy. Current heart failure reports, 12(5), 302-308.

Rabaeus, Mikael, Paul V. Nguyen, and Michel de Lorgeril. Recent flaws in Evidence Based Medicine: statin effects in primary prevention and consequences of suspending the treatment. Journal of Controversies in Biomedical Research3.1 (2017): 1-10.

Richards, Suzanne H., et al. Psychological interventions for coronary heart disease: Cochrane systematic review and meta-analysis. European journal of preventive cardiology25.3 (2018): 247-259.

Sabatine, Marc S., et al. Evolocumab and clinical outcomes in patients with cardiovascular disease. New England Journal of Medicine 376.18 (2017): 1713-1722.

Sofi, Francesco, et al. Insomnia and risk of cardiovascular disease: A meta-analysis. European journal of preventive cardiology 21.1 (2014): 57-64.

Suls, J. (2018). Toxic affect: Are anger, anxiety, and depression independent risk factors for cardiovascular disease?. Emotion Review, 10(1), 6-17.

Targher, G., Day, C. P., & Bonora, E. (2010). Risk of cardiovascular disease in patients with nonalcoholic fatty liver disease. New England Journal of Medicine, 363(14), 1341-1350.

Vancheri, Federico, et al. Time trends in statin utilisation and coronary mortality in Western European countries. BMJ open6.3 (2016): e010500.

Wulsin, L. R., & Singal, B. M. (2003). Do depressive symptoms increase the risk for the onset of coronary disease? A systematic quantitative review. Psychosomatic medicine, 65(2), 201-210.

Articolul Cholesterol lowering, between laziness & superficiality apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

However, as I encourage all of my patients to be, I also invite you to be skeptical and read – of course, or not – the studies quoted in these articles. And although it is just an invitation to understand that animal protein in general and dairy products in particular are not carcinogenic, please take into consideration that regardless of long-held personal beliefs these foods consumption by patients diagnosed with cancer is helping them achieve better prognosis by supporting the effectiveness of oncology treatment and by counteracting side effects.

Epidemiological studies that analyse the carcinogenicity of meat consumption are made by evaluating the responses given by the respondents in that study compared to those who have declared that they have consumed and those who have declared that they have not consumed meat. There are answers given by some people questioned and believed on their given word. So the results of epidemiological studies:

• don’t show causality, epidemiology studies simply pointing out risk factors for the population questioned within that particular study – Ananth & Schisterman, 2017
• may differ from one study to another, depending on the actual memory and honesty of the individuals questioned in each particular study about what they have consumed in their youth or 1 year ago – a phenomenon long known and called „recall bias“ – Chavarro et al., 2009
• can be easily manipulated by omitting various bias factors, depending on the honesty, financial interests and personal beliefs of the researchers publishing these questionnaire studies – de Abreu Silva & Marcadenti, 2009; Fogelholm, Kanerva & Männistö, 2015

Starting from the fact that epidemiology is based, however, on the honesty of both researchers and study participants, there still remain two semantic issues – generated by the fact that the respondents answer the questions of the epidemiologists by basically reading words in a questionnaire.

1. How do we define the word “cancer”?

In most questionnaires, “cancer” is a diagnosis, but today we know there are countless completely different diseases called “cancer”.

– So eating any type of meat increases the risk of any type of cancer?

On specific types of cancer, studies indicate that:

1. red or processed meat intake does not associate increased risk of renal cancer – Alexander & Cushing, 2009
2. red meat intake does not associate increased risk of lung cancer – Gnagnarella et al., 2018
3. meat intake is not associated with increased risk of multiple myeloma – Alexander et al., 2007
4. meat intake does not associate an increased risk of prostate cancer – Bylsma & Alexander, 2015
5. meat intake does not associate an increased risk of ovarian cancer – Crane et al., 2013
6. the excessive intake of deli meats like sausage and hamburgers associates an increased risk of breast cancer, not the consumption of red meat in itself – Anderson et al, 2018; Boldo et al., 2018
7. it is questionable if the risk of childhood brain cancer is associated or not with the consumption of sausage, hamburger or hotdogs by pregnant women – Pogoda & Preston-Martin, 2001;Huncharek, 2011; Henshaw & Suk, 2015
8. excessive intake of red meat associates the increased risk of digestive cancers, but this correlation differs from one digestive segment to another:
   • excessive red meat consumption associates an increased risk of esophageal cancer – Salehi et al., 2013
   • the evidence that supports an the increased risk of gastric cancer by eating red meat, sausages or precooked meat – Zhao, Yin & Zhao, 2017
   • there are sufficient epidemiological associations to support the increased risk of colorectal cancer by excessive consumption of red meat (Chan et al., 2011), although some studies point out that association seems to be valid only in distal colon cancer (Larsson et al., 2005; Bernstein et al., 2015)
   • excessive red meat consumption does appear to increase the risk of pancreatic cancer in men, but not in women, and the correlation is inconsistent and only shows related to excessive intake not with normal intake – Zhao et al., 2017
   • meat consumption is not correlated with an increased risk of liver cancer – Fedirko et al., 2013

2. How do we define the word “meat”?

Beef steak, turkey stew, pork meatball soup, grilled lamb, “mici” (a Romanian dish made from minced meat), chicken soup, hotdogs, hamburgers, schnitzels and the famous hot wings flying out of the overly used hot oil directly into the garlic mayonnaise – all are often put comfortably under the same “meat” label.

– But is Angus beef steak as carcinogenic as the hotdogs? 

– Or the Mangalita pork meat as carcinogenic as the hamburger? And what if the hamburger is made of Angus beef? 

– And what about quail, cock or pheasant meat?

The best answer based on „I will tell the truth, the whole truth, and nothing but the truth, so help me God“ is that we simply don’t know. Some giraffes want to see only green in front of their eyes, some ostrich – just sand.

What we know – at large – on specific types of meat is that:

1. “white meat” intake does not increase or associate a moderate decrease in the risk of “cancer” – Kolahdooz et al., 2010; Maragoni et al., 2015; Etemadi et al., 2017
2. “red meat” intake correlates with an increased risk of “cancer” – Domingo and Nadal, 2017

The words “white meat” generally define chicken, turkey or other poultry and fish. And the words “red meat” define generically “processed red meat” and “unprocessed red meat”.

– Now is all the red meat carcinogenic, no matter how little we consume?

First of all, any type of meat may be biologically pink or red depending on how sedentary that particular animal was (visible to the naked eye, looking at the piece of meat on our plate, or visible on the microscope, looking at the number and type of muscle fibres in the meat). Even wild fish has more red meat than farmed fish, simply because it swims more. Defining meat as white or red based on the species is pretty shallow.

Secondly, the words “processed red meat” generically define precooked products made of meat that has already been minced, such as hamburgers, hotdogs, salami, sausages, canned meat, liver pate, and fast food meat products. And the words “unprocessed red meat” generally define home cooked beef, sheep, pork and game meat, industrially unprocessed.

Studies that separate “red processed meat” from “red unprocessed meat” contradict the generic link between “red meat” and “cancer” (Larsson and Orsini, 2013; Anderson et al., 2018).

A systematic analysis published by Carr et al. in 2016 in International Journal of Cancer indicates that unprocessed red meat the normal intake does not increase the risk of cancer, not even in the case of colorectal cancer. This analysis shows that, in order to associate an increased in risk, the consumption of unprocessed red meat must be excessive and that the consumption of pork meat does not involve the increase of risk even when excessive, the risk being increased only by excessive consumption of beef or lamb.

Systematic analyzes that examined the association between the heterocyclic amines, polycyclic aromatic hydrocarbons or benzopyrene, formed in meat during cooking, and the carcinogenic impact of hem iron indicate only poor associations between red and processed meat consumption and increased risk of cancer (Kuratko et al., 2016).

So, the current scientific literature shows that:

1. Generally, moderate “meat” consumption does not associate an increased “cancer” risk.
2. Particularly, the consumption processed meat and the excessive consumption of beef or lamb meat are associated with an increase in the risk of certain types of cancer.

The problem with nutrition these days is that anyone who can chew is a nutritionist undercover, thus at the diametrically opposite pole of those recommending to cancer patients to avoid meat consumption, are the ones recommending to cancer patients to start a ketogenic diet – diet based on keeping carbohydrates intake as low as possible, “low intake” defined solely on the imagination residing within the self-proclaimed nutritionist’s pen. Nope, it’s not Dukan or Atkins, it’s pure Gigica diet, strictly tailored for you with tons of meat meant to starve away cancer.

The studies quoted in this article support the moderate consumption of lightly cooked or boiled meat as part of a healthy diet similar to the Mediterranean diet, not the recommendation of ketogenic diet for cancer patients – a recommendation made by those who elegantly offer illusions to cancer patients, understanding superficially or at all the oncological consequences of this extreme diet.

In my fourth book, I present in detail – with scientific arguments – that the ketogenic diet associates an increased risk of metastasis and recurrence, an increase in tumor aggression and the development of resistance to oncological treatment.

This is based on the current scientific data which:

1. contraindicates ketogenic diet in any patient diagnosed with cancer (Erickson et al., 2017)
2. recommends moderate meat consumption as part of a variety of dairy, cheese, eggs, fish, fruits, vegetables, seeds, grains, whole grains and quality oils (Schwingshackl & Hoffmann, 2014)

Moderate intake of high quality meat cooked the right way, not hotdogs or schnitzels eaten on the run.

Quoted studies

Alexander, Dominik D. et al. “Multiple myeloma: a review of the epidemiologic literature.” International journal of cancer 120.S12 (2007): 40-61.

Alexander, D. D., & Cushing, C. A. (2009). Quantitative assessment of red meat or processed meat consumption and kidney cancer. Cancer detection and prevention, 32(5), 340-351.

Ananth, C. V., & Schisterman, E. F. (2017). Confounding, causality, and confusion: the role of intermediate variables in interpreting observational studies in obstetrics. American journal of obstetrics and gynecology, 217(2), 167.

Anderson, Jana J. et al. “Red and processed meat consumption and breast cancer: UK Biobank cohort study and meta-analysis.” European Journal of Cancer 90 (2018): 73-82.

Bernstein, Adam M. et al. “Processed and unprocessed red meat and risk of colorectal cancer: analysis by tumor location and modification by time.” PloS one 10.8 (2015): e0135959.

Boldo, Elena, et al. “Meat intake, methods and degrees of cooking and breast cancer risk in the MCC-Spain study.” Maturitas 110 (2018): 62-70.

Bylsma, L. C., & Alexander, D. D. (2015). A review and meta-analysis of prospective studies of red and processed meat, meat cooking methods, heme iron, heterocyclic amines and prostate cancer. Nutrition journal, 14(1), 125.

Carr, Prudence R. et al. “Meat subtypes and their association with colorectal cancer: Systematic review and meta‐analysis.” International journal of cancer 138.2 (2016): 293-302.

Chan, Doris SM et al. “Red and processed meat and colorectal cancer incidence: meta-analysis of prospective studies.” PloS one 6.6 (2011): e20456.

Chavarro, Jorge E. et al. “Validity of adolescent diet recall 48 years later.” American journal of epidemiology 170.12 (2009): 1563-1570.

Crane, Tracy E. et al. “Dietary intake and ovarian cancer risk: a systematic review.” Cancer Epidemiology and Prevention Biomarkers (2013): cebp-0515.

de Abreu Silva, Erlon Oliveira, and Aline Marcadenti. “Higher red meat intake may be a marker of risk, not a risk factor itself.” Archives of internal medicine 169.16 (2009): 1538-1539.

Domingo, J. L., & Nadal, M. (2017). Carcinogenicity of consumption of red meat and processed meat: A review of scientific news since the IARC decision. Food and Chemical Toxicology, 105, 256-261.

Erickson, N. et al. “Systematic review: isocaloric ketogenic dietary regimes for cancer patients.” Medical Oncology 34.5 (2017): 72.

Etemadi, Arash et al. “Mortality from different causes associated with meat, heme iron, nitrates, and nitrites in the NIH-AARP Diet and Health Study: population based cohort study.” bmj 357 (2017): j1957.

Fogelholm, M., Kanerva, N., & Männistö, S. (2015). Association between red and processed meat consumption and chronic diseases: the confounding role of other dietary factors. European journal of clinical nutrition, 69(9), 1060.

Gnagnarella, Patrizia et al. “Carcinogenicity of High Consumption of Meat and Lung Cancer Risk Among Non-Smokers: A Comprehensive Meta-Analysis.” Nutrition and cancer 70.1 (2018): 1-13.

Fedirko, V. et al. “Consumption of fish and meats and risk of hepatocellular carcinoma: the European Prospective Investigation into Cancer and Nutrition (EPIC).” Annals of oncology 24.8 (2013): 2166-2173.

Henshaw, D. L., & Suk, W. A. (2015). Diet, transplacental carcinogenesis, and risk to children.

Huncharek, Michael. “Maternal Dietary Intake of N-Nitroso Compounds from Cured Meat and the Risk of Pediatric Brain Tumors.” Handbook of Behavior, Food and Nutrition. Springer, New York, NY, 2011. 1817-1831.

Kolahdooz, Fariba et al. “Meat, fish, and ovarian cancer risk: results from 2 Australian case-control studies, a systematic review, and meta-analysis–.” The American journal of clinical nutrition 91.6 (2010): 1752-1763.

Kuratko, Connye et al. “Systematic Reviews of Current Literature Fail to Establish Dietary Benzo [a] pyrene, Heterocyclic Aromatic Amines, or Heme Iron as Mechanisms Linking Red and Processed Meat Consumption with Cancer Risk.” The FASEB Journal 30.1 Supplement (2016): 1167-5.

Marangoni, Franca, et al. “Role of poultry meat in a balanced diet aimed at maintaining health and wellbeing: an Italian consensus document.” Food & nutrition research 59.1 (2015): 27606.

Larsson, Susanna C., et al. “Red meat consumption and risk of cancers of the proximal colon, distal colon and rectum: the Swedish Mammography Cohort.” International journal of cancer113.5 (2005): 829-834.

Larsson, S. C., & Orsini, N. (2013). Red meat and processed meat consumption and all-cause mortality: a meta-analysis. American journal of epidemiology, 179(3), 282-289.

Pogoda, J. M., & Preston-Martin, S. (2001). Maternal cured meat consumption during pregnancy and risk of paediatric brain tumour in offspring: potentially harmful levels of intake. Public health nutrition, 4(2), 183-189.

Salehi, Maryam et al. “Meat, fish, and esophageal cancer risk: a systematic review and dose-response meta-analysis.” Nutrition reviews 71.5 (2013): 257-267.

Schwingshackl, L., & Hoffmann, G. (2014). Adherence to Mediterranean diet and risk of cancer: A systematic review and meta‐analysis of observational studies. International journal of cancer, 135(8), 1884-1897.

Zhao, Zhanwei et al. “Association between consumption of red and processed meat and pancreatic cancer risk: a systematic review and meta-analysis.” Clinical Gastroenterology and Hepatology 15.4 (2017): 486-493.

Zhao, Z., Yin, Z., & Zhao, Q. (2017). Red and processed meat consumption and gastric cancer risk: A systematic review and meta-analysis. Oncotarget, 8(18), 30563.

Articolul Is meat carcinogenic? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Really! I saw with my own eyes how they cooked together during a Christmas TV show some potatoes with turkey meat that looked so absolutely marvellous that one could eat the TV.

Probably neither my mother nor Jamie’s mother had heard of Montignac or of the gastric juice diluting in the stomach if you drink water while you eat, still apparently some of us grew up with this combination sold as pure heresy by so many self-declared Google University graduates.

And I write “apparently some of us” because, although I think we all grew up with potatoes and meat, nowadays it looks like some started to argue their parents for not knowing basic things like the one stating potato should not be eaten together with meat. Their parents messed up the metabolism they are trying so hard to fix by finally consuming the protein and the carbohydrate separately and by drinking water at least half an hour after eating to not dilute the juice.

– What juice?

– One, that one, why do you need to ask?!

Digestion of potato starch begins in the mouth, under the action of salivary amylase, stops in the stomach and restarts in the small intestine, under the action of pancreatic amylase, no matter what other foods you eat at that meal.

Digestion of the fat from the butter and milk used to cook mashed potatoes begins in the stomach and mainly takes place in the small intestine, under the action of pancreatic lipase after being emulsified by bile salts, no matter what other foods you eat at that meal.

Digestion of meat proteins begins in the stomach and takes place in the small intestine under the action of pancreatic proteases, no matter what other foods you eat at that meal.

And no matter what you eat at that meal, the main thing that happens to food within the stomach is mechanical digestion because the stomach works just like a blender, mixing very well all the gastric content.

The idea that some things are digested earlier and others later, or that some things do not digest well because you have combined them with something can be a good subject for a glass of wine chat when you’re imagination runs low, but the stomach digestion result is gastric chyme – a homogeneous semi-liquid mixture of nutrients, less than 0.5 mm in diameter, which is gradually eliminated as small amounts through the pylorus canal in the small intestine.

The main role of the stomach is mechanical digestion.

Nothing rots or ferments in the stomach, because these two processes can only be performed by bacteria, and there are no bacteria in the stomach.

Or, if you painfully feel that in your own and personal stomach are some bacteria, you are warmly invited to the gastroenterologist for a Helicobacter pylori test and proper treatment.

And for God’s sake, if one could dilute the gastric juice by drinking water while eating, no one would even need omeprazole.

And if you’re experiencing bloating after eating, avoid eating too much and please don’t nibble in between meals. No fruit snacks, no coffee, gum or other nibbling, because such behaviour disrupts satiety hormones secretion, influencing metabolism and digestive motility.

The glucose, fructose, galactose, fatty acids and amino acids are the result of the intestinal – not gastric –digestion. And intestinal digestion is the same for all pancreas owners.

– So, did my mother and Jamie’s mother ate potatoes and meat at the same meal because they knew they have a pancreas = internal organ secreting amylase, lipase, and proteases (enzymes perfectly capable to digest any food combination – and even the pancreas itself in case of an acute pancreatitis for example)?

– Nope, I do not think they knew all this.

They probably ate potatoes and meat at the same meal and fed as with such delicious foods because, after such a meals we all felt good.

P.S. To all pseudo-nutritionists out there or to people who believe that the entire world’s gastronomy is completely fucked up I cordially recommend reading Illustrated Biochemistry. It helps weed out the non-sense.

Articolul Potatoes + meat = LOVE apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Some research shows that the use of artificial sweeteners is associated with a modest weight loss (2).

Other research shows that the use of artificial sweeteners is associated with weight gain (3,4, 5, 6, 7, 8).

Everyone says they are right (9).

Just that, besides weight loss or weight gain, the use of artificial sweeteners is also associated with:

1. glucose intolerance induced by dysbiosis (10,11, 12, 13, 14)
2. diabetes (15, 16, 17, 18, 19, 20, 21)
3. cardiovascular disease (22, 23, 24, 25, 26)

And also, starting 2012 artificial sweeteners are recognised as environmental contaminants (27, 28, 29).

So, don’t worry = no sugar?

References

(1) Shankar, Padmini, Suman Ahuja, and Krishnan Sriram. “Non-nutritive sweeteners: review and update.” Nutrition 29.11 (2013): 1293-1299).

(2) Miller, Paige E., and Vanessa Perez. “Low-calorie sweeteners and body weight and composition: a meta-analysis of randomized controlled trials and prospective cohort studies.” The American journal of clinical nutrition 100.3 (2014): 765-777.

(3) Fowler, Sharon PG, Ken Williams, and Helen P. Hazuda. “Diet soda intake is associated with long‐term increases in waist circumference in a biethnic cohort of older adults: The San Antonio longitudinal study of aging.” Journal of the American Geriatrics Society 63.4 (2015): 708-715.

(4) Pliego-Rivero, F. Bernardo, et al. “The Non-Caloric Sweeteners Aspartame, Sucralose and Stevia sp. Induce Specific but Differential Responses to Compartmentalized Adipose Tissue Accumulation.” The FASEB Journal 31.1 Supplement (2017): 639-46.

(5) Polyák, Éva, et al. “Effects of artificial sweeteners on body weight, food and drink intake.” Acta Physiologica Hungarica 97.4 (2010): 401-407.

(6) Meni, Allison C. Sylvetsky, Susan E. Swithers, and Kristina I. Rother. “Positive association between artificially sweetened beverage consumption and incidence of diabetes.” Diabetologia 58.10 (2015): 2455-2456.

(7) Yang Qing. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. The Yale journal of biology and medicine, 2010, 83.2: 101.

(8) Simon, Becky R., et al. “Artificial sweeteners stimulate adipogenesis and suppress lipolysis independently of sweet taste receptors.” Journal of Biological Chemistry 288.45 (2013): 32475-32489.

(9) Mandrioli, Daniele, Cristin E. Kearns, and Lisa A. Bero. “Relationship between research outcomes and risk of bias, study sponsorship, and author financial conflicts of interest in reviews of the effects of artificially sweetened beverages on weight outcomes: a systematic review of reviews.” PloS one 11.9 (2016): e0162198.

(10) Bokulich, Nicholas A., and Martin J. Blaser. “A bitter aftertaste: unintended effects of artificial sweeteners on the gut microbiome.” Cell metabolism 20.5 (2014): 701-703.

(11) Suez, J., Korem, T., Zeevi, D., Zilberman-Schapira, G., Thaiss, C. A., Maza, O., … & Kuperman, Y. (2014). Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature, 514(7521), 181-186.

(12) Nettleton, Jodi E., Raylene A. Reimer, and Jane Shearer. “Reshaping the gut microbiota: Impact of low calorie sweeteners and the link to insulin resistance?.” Physiology & behavior 164 (2016): 488-493.

(13) Pepino, M. Yanina. “Metabolic effects of non-nutritive sweeteners.” Physiology & behavior 152 (2015): 450-455.

(14) Swithers, Susan E. “Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements.” Trends in Endocrinology & Metabolism 24.9 (2013): 431-441.

(15) Nettleton, Jennifer A., et al. “Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA).” Diabetes care 32.4 (2009): 688-694.

(16) Fagherazzi, Guy, et al. “Consumption of artificially and sugar-sweetened beverages and incident type 2 diabetes in the Etude Epidémiologique auprès des femmes de la Mutuelle Générale de l’Education Nationale–European Prospective Investigation into Cancer and Nutrition cohort.” The American journal of clinical nutrition 97.3 (2013): 517-523.

(17) Greenwood, D. C., et al. “Association between sugar-sweetened and artificially sweetened soft drinks and type 2 diabetes: systematic review and dose–response meta-analysis of prospective studies.” British Journal of Nutrition 112.05 (2014): 725-734.

(18) Yarmolinsky, James, et al. “Artificially Sweetened Beverage Consumption Is Positively Associated with Newly Diagnosed Diabetes in Normal-Weight but Not in Overweight or Obese Brazilian Adults.” The Journal of nutrition 146.2 (2016): 290-297.

(19) Fagherazzi, Guy, et al. “Chronic Consumption of Artificial Sweetener in Packets or Tablets and Type 2 Diabetes Risk: Evidence from the E3N-European Prospective Investigation into Cancer and Nutrition Study.” Annals of Nutrition and Metabolism 70.1 (2017): 51-58.

(20) Meni, Allison C. Sylvetsky, Susan E. Swithers, and Kristina I. Rother. “Positive association between artificially sweetened beverage consumption and incidence of diabetes.” Diabetologia 58.10 (2015): 2455-2456.

(21) Hoffmann, Brian R., and Andrew S. Greene. “Mechanisms of Vascular Endothelial Dysfunction: The Problem with Sugar and Artificial Sweeteners.” The FASEB Journal 31.1 Supplement (2017): 853-9.

(22) Cheungpasitporn, Wisit, et al. “Sugar and artificially sweetened soda consumption linked to hypertension: a systematic review and meta-analysis.” Clinical and Experimental Hypertension 37.7 (2015): 587-593.

(23) Narain, Aditya, C. S. Kwok, and M. A. Mamas. “Soft drinks and sweetened beverages and the risk of cardiovascular disease and mortality: a systematic review and meta‐analysis.” International journal of clinical practice 70.10 (2016): 791-805.

(24) Wersching, Heike, Hannah Gardener, and Ralph L. Sacco. “Sugar-Sweetened and Artificially Sweetened Beverages in Relation to Stroke and Dementia.” (2017): 1129-1131.

(25) Gardener, Hannah, et al. “Diet soft drink consumption is associated with an increased risk of vascular events in the Northern Manhattan Study.” Journal of general internal medicine 27.9 (2012): 1120-1126.

(26) J., Beiser, A. S., Aparicio, H. J., Satizabal, C. L., Vasan, R. S., … & Jacques, P. F. (2017). Sugar-and Artificially Sweetened Beverages and the Risks of Incident Stroke and Dementia. Stroke, STROKEAHA-116.

(27) Scheurer, Marco, Heinz-J. Brauch, and Frank T. Lange. “Analysis and occurrence of seven artificial sweeteners in German waste water and surface water and in soil aquifer treatment (SAT).” Analytical and bioanalytical chemistry 394.6 (2009): 1585-1594.

(28) Sang, Ziye, et al. “Evaluating the environmental impact of artificial sweeteners: a study of their distributions, photodegradation and toxicities.” Water research 52 (2014): 260-274.

(29) Lange, F. T., Scheurer, M., & Brauch, H. J. (2012). Artificial sweeteners—a recently recognized class of emerging environmental contaminants: a review. Analytical and Bioanalytical Chemistry, 403(9), 2503-2518.

Articolul Don’t worry = No sugar? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Some researchers have suggested that red wine is the reason of the superiority of the French’s cardiovascular health, others have contradicted them, arguing that the beneficial effect is due to ethanol from any alcoholic beverage, and others have contradicted everyone, claiming that ethanol consumed in any dose is toxic to the body. So, who’s right?

1. What does „moderate alcohol consumption“ mean?

The effects of alcohol consumption vary depending on age, gender and health status, and also on the amount consumed and on the frequency of consumption. For overall healthy people, whose age, genetics, pregnancy, illness or medication do not prohibit alcohol consumption, the definition of moderate consumption is relatively fluid.

Moderate alcohol consumption is defined by the upper limit, over which the benefits of alcohol are outweighed by the harmful effects. In agreement with this common sense definition, moderate alcohol consumption was set at:

• 1 drink per day for women
• 2 drinks per day for men.

A standard beverage contains, on average, 12-14 g of pure alcohol: 0.5 l of beer, 0.25 l of wine, or about 50 ml of brandy, vodka or whiskey (5).

– How often can we drink alcohol, under the definition of “moderate alcohol consumption”?

At the population level, moderate alcohol consumption may vary:

• from an alcoholic drink a day associated with one or both main meals (>50-100 g ethanol per week) in France,
• up to 7-14 drinks per day (> 70-140 g ethanol) in Ireland and in practically any country with people having compulsive alcohol intake only on weekends or holidays (6).

And although both patterns of consumption fall within the definition of moderate alcohol consumption, the second typology (“binge drinking” or “compulsive alcohol consumption”) is extremely dangerous, leading from acute poisoning with alcohol to alcohol coma or death (7).

– Which alcoholic drinks are healthier?

The role of wine in explaining the French paradox is questionable because, statistically, the beneficial effects of active substances in wine arise from a high wine consumption (8).

Some studies suggest that red wine is beneficial (9).

Other studies – that wine of any color and beer offer cardiovascular benefits superior to spirits drinks(10).

And other studies suggest that ethanol in any alcoholic drink produces the same cardiovascular effects (11).

2. What are the positive effects of moderate alcohol consumption?

Apparently, the hypothesis that moderate alcohol consumption prevents cardiovascular disease and decreases the incidence of mortality from this cause seems to make sense. Epidemiological evidence suggests a J-shaped relationship (Figure 1) between alcohol consumption and mortality (12).

Figure 1. DiCastelnuovo et al. Alcohol dosing and total mortality, 2006.

The mechanisms behind the protective effects could be:

• increasing the blood level of high density lipoproteins cholesterol (HDL-c),
• lowering the blood level of low density lipoproteins cholesterol (LDL-c),
• preventing the blood clots formation by reducing platelet aggregation.

Thus, moderate alcohol consumption might reduce cardiovascular risk, both by inhibiting atheromatosis, and by lowering the blood coagulation rate.

– Does moderate alcohol consumption increase HDL-cholesterol?

An HDL-c blood level below 40 mg/dl is associated with an increased risk of cardiovascular disease, even in people whose total cholesterol and LDL-c blood levels are within the normal range (13).

HDL-c between 40 and 60 mg/dl is considered “neutral” and does not affect cardiovascular risk.

And HDL-c above 60 mg/dl is associated with a reduced cardiovascular risk – representing the goal for prophylaxis of the cardiovascular disease.

We can increase HDL-c by:

• quitting smoking,
• decreasing the percentage of body fat
  • through regular sports, and
  • through a diet based on:
    • increased fiber, omega-3 fatty acids and antioxidants intake
    • reducing or eliminating trans fats (14).

Studies suggest that moderate alcohol consumption reduces the risk of atherosclerosis and the main mechanism seems to be the ability to increase HDL-c concentration (15). However, the mechanisms by which alcohol determines thisHDL-c increase are not fully understood.

Some researchers have suggested that alcohol increases HDL cholesterol by increasing the transport rate of apolipoproteins A-I and A-II (16). Others have explained the effect by stimulating cells’ cholesterol efflux and its esterification in plasma (17).

However, regardless of the mechanism by which moderate alcohol consumption increases HDL-c, moderate alcohol consumption still contributes to an increased triglycerides blood level (18). And the increase of the triglycerides blood level is an independent risk factor for cardiovascular disease (19).

– Does moderate alcohol consumption lower LDL-cholesterol?

The effects of moderate alcohol consumption on blood levels of LDL-c are unclear.

From studies that found only a small LDL-c lowering effect of only 0.1 mmol/l, following a daily consumption of 15-30 g of alcohol per day for 8 weeks (20), to studies that found a hypolipidemic effect in young people only, and the opposite effect, of increasing LDL-c, in elderly adults (21), to studies that found LDL-c decreases only for moderate daily alcohol consumption, and the opposite effect, of increasing LDL-c, for moderate but compulsive consumption (22) – the many conclusions of scientists are very contradictory, sounding more like assumptions and biased personal opinions than science.

On the other hand, a 2003 study showed that dealcoholised wine has an LDL-c lowering effect similar to atorvastatin (Lipitor), 20% higher than that of natural alcohol – suggesting that ethanol in wine actually masks the hypolipidemic effect of polyphenols (23).

So we’re back to the question: is the alcohol or the polyphenol within a Mediterranean diet the basis for the famous French paradox?

– Does moderate alcohol consumption have antithrombotic effects?

In addition to influencing the LDL-c / HDL-c ratio, moderate alcohol consumption affects coagulation factors (fibrinogen, coagulation factor VII and von Willebrand factor), thus having antithrombotic effects (24).

However, Rantakömi et al. showed that  overweight and hypertensive patients with moderate alcohol consumption have an increased risk of ischemic stroke compared to those who don’t drink (25).

The obesity epidemic should therefore be counted in before recommending moderate alcohol consumption as a means of cardiovascular prevention.

Also, compulsive alcohol consumption is associated with inhibition of fibrinolysis, which contributes to the unstable balance between moderate alcohol consumption and cardiovascular mortality (26).

3. What are the negative effects of moderate alcohol consumption?

Any benefits of moderate alcohol consumption on mortality are abolished at an excessive consumption level by increasing the risk of death due to:

• alcoholic cardiopathy,
• paroxysmal tachycardia,
• depression,
• cancer,
• cirrhosis,
• traffic accidents.

– Does moderate alcohol consumption have arrhythmic effects?

Atrial fibrillation (AF) is the most common cardiac arrhythmia, and the close relationship between compulsive alcohol and AF (even in healthy people) has been known for decades. Of course, the causal relationship is directly proportional to the dose, but the amount of alcohol needed to increase the risk of AF is only of 2 alcoholic drinks a day for women and 4 for men (27).

So, simply doubling the amount of 1 drink per day in women and 2 in men increases the risk of atrial fibrillation.

Also, regular alcohol intake has cumulative effects, potentially affecting left ventricular function of the heart long before cardiac abnormalities become symptomatic.

Thus, moderate alcohol consumption depresses cardiovascular function, the deterioration progressing:

• from the isolated impairment of the heart muscle pump function
• to cardiomegaly and, finally,
• to decompensation (28).

– Does moderate alcohol consumption have hepatotoxic effects?

Paradoxically, the hepatic effects of moderate alcohol consumption are even more controversial than cardiac effects.

On one hand, some studies show a beneficial effect of moderate alcohol consumption, associating a low incidence of liver steatosis:

• both in healthy people (29),
• as well as in people with high cardiac risk (30).

On the other hand, the so-called hepatic alcohol benefits are considered by many clinicians purely epidemiological (31).

Also, a study of 18,899 people aged 25 to 74 demonstrated that:

• men over the age of 40 who consumed over 8 alcoholic drinks per week  – but remained within the moderate 7-14 permitted drinking range for males – had elevated liver transaminases, despite the lack of any symptoms;
• in men under 40, the effect occurs at a consumption of 14 alcoholic beverages per week (32).

– Does moderate alcohol consumption have carcinogenic effects?

Studies show an obvious causal link between excessive alcohol and cancer (33).

However, it seems that also moderate alcohol consumption can be carcinogenic (34).

Different factors may contribute to the pathogenesis of cancer associated with moderate alcohol consumption, including the actions of acetaldehyde, the most toxic metabolite of alcohol. Acetaldehyde itself is carcinogenic, being used to generate cancer in laboratory animals. In addition, highly reactive molecules that are generated during alcohol metabolism can damage DNA, thus increasing the carcinogenic potential of acetaldehyde (35).

Moderate alcohol consumption is responsible for the increased risk of digestive tract cancers (36). And, in addition to the carcinogenic potential, regardless of the type and dose of alcohol consumed, alcohol facilitates the occurrence of gastroesophageal reflux disease by reducing lower esophageal sphincter pressure and esophageal motility.

Another type of cancer strongly associated epidemiologically with moderate alcohol consumption is breast cancer, both in women and men – a fact ignored by the recommendation that moderate alcohol consumption is part of a healthy lifestyle (37).

4. What are the bias factors in studies researching the effects of moderate alcohol consumption?

Many studies on the effects of moderate alcohol consumption have produced highly contradictory results (38).

– What are the bias factors responsible for these contradictory results?

Some of the causes of these contradictory results may be the design of the study and the hidden variables, sometimes more significant in inducing the epidemiological results than the presumed causal variables of the study.

An objective study on the effects of ethanol should be:

• controlled randomized – subjects shared randomly as non-alcohol users, moderate consumers, compulsive and alcoholic consumers, with no difference between groups other than the variables to be studied,
• double-blind – neither subjects nor researchers will know who receives alcohol and who receives placebo,
• longitudinal – to study the same subjects over time
• performed on a sufficiently long term – subjects should not change the pattern of alcohol consumption throughout the study to continue to be part of the group they were originally classified in.

The cost and logistics of such a study are the reasons cited in support of the fact that these studies are based on individual (often retrospective) reports and on the subjective definitions of groups of participants – methods that do not guarantee the accuracy of the data collected (39).

The definition of abstainers (non-alcohol users) in many studies refers only to people who did not consume alcohol in the last month (40).

Thus, it is not surprising that the group of moderate alcohol consumers is healthier than the group of abstainers – if we introduce them under the generic name of “abstainers”:

• former alcoholics – with an increased risk of ischemic cardiopathy, hypertension, diabetes, ulcer, biliary dyskinesia and bronchitis
• sick people – whose illness or medication prevented them from consuming alcohol in the month prior their enrolling in the study.

The bad health condition of many people in the group of abstainers should not be evidence of the benefits of drinking (41).

However, even in studies in which abstinence includes people who have not consumed alcohol for one year, the inclusion of former alcoholics is tendentious, because former alcoholics have a cardiovascular risk of up to twice as high.

The association between moderate alcohol consumption and cardiac protection disappears after the former alcoholics are removed from the group of abstainers (42).

It is true that an alcoholic beverage can increase the mood and palatability of the foods consumed at the meal, but the real problem is that very few people consume alcohol in moderation – most either completely avoids alcohol for days and then consumes too much once or consumes more than moderate each time (43).

Attempting to promote moderate alcohol consumption among abstainers and to somehow excuse it among more or less moderate consumers is healthy for the alcohol industry.

But for people, the benefits more fluid.

Quoted studies

1. Black S. Clinical and Pathological Reports. Newry, UK: Alex Wilkinson, 1819, p. 1–47.
2. St. Leger AS, Cochrane AL, Moore F. Factors associated with cardiac mortality in developed countries with particular reference to the consumption of wine. Lancet 1: 1018–1020, 1979.
3. Casswell S. Public discourse on the benefits of moderation: implications for alcohol policy development. Addiction, 88(4), 459-465, 1993.
4. The top 10 causes of death. (Updated July 2013) http://www.who.int/mediacentre/factsheets/fs310/en/index.html
5. National Institute on Alcohol Abuse and Alcoholism. Helping patients who drink too much: A clinician’s guide (updated) Washington, DC: National Institutes of Health; 2007. NIH Publication No. 07-3769.
6. Ruidavets, Jean-Bernard et al. Patterns of alcohol consumption and ischaemic heart disease in culturally divergent countries: The Prospective Epidemiological Study of Myocardial Infarction (PRIME). BMJ: British Medical Journal 341 (2010). doi: http://dx.doi.org/10.1136/bmj.c6077
7. 3.1.3. Mukamal K.J., Conigrave K.M., Mittleman M.A., Camargo CA. Jr., Stampfer M.J., Willett W.C., Rimm E.B. Roles of drinking pattern and type of alcohol consumed in coronary heart disease in men. N Engl J Med 348: 109–118, 2003.
8. Holahan, C. J., Schutte, K. K., Brennan, P. L., North, R. J., Holahan, C. K., Moos, B. S., & Moos, R. H. (2012). Wine consumption and 20-year mortality among late-life moderate drinkers. Journal of studies on alcohol and drugs,73(1), 80.
9. Streppel M. T., Ocké M. C., Boshuizen H. C., Kok F. J., & Kromhout D. (2009). Long-term wine consumption is related to cardiovascular mortality and life expectancy independently of moderate alcohol intake: the Zutphen Study. Journal of epidemiology and community health, 63(7), 534-540. doi:10.1136/jech.2008.082198.
10. Costanzo S., Di Castelnuovo A., Donati M. B., Iacoviello L., & de Gaetano G. (2011). Wine, beer or spirit drinking in relation to fatal and non-fatal cardiovascular events: A meta-analysis. European journal of epidemiology, 26(11), 833-850.
11. Krnic M., Modun D., Budimir D., Gunjaca G., Jajic I., Vukovic J., … & Boban M. (2011). Comparison of acute effects of red wine, beer and vodka against hyperoxia-induced oxidative stress and increase in arterial stiffness in healthy humans. Atherosclerosis, 218(2), 530-535. http://dx.doi.org/10.1016/j.atherosclerosis.2011.07.004
12. DiCastelnuovo A., Castanzo S., Bagnardi V., Donati M.B., Iacoviello L., de Gaetano G. Alcohol dosing and total mortality in men and women. Arch Intern Med. 166 2006:2437-2445.
13. Cui Y., Blumenthal R. S., Flaws J. A., Whiteman M. K., Langenberg P., Bachorik P. S., & Bush T. L. (2001). Non-high-density lipoprotein cholesterol level as a predictor of cardiovascular disease mortality. Archives of Internal Medicine, 161(11), 1413. doi:10.1001/archinte.161.11.1413.
14. O’Donnell Martin J., et al. Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): A case-control study. The Lancet 376.9735 (2010): 112-123.
15. Boden, William E. High-density lipoprotein cholesterol as an independent risk factor in cardiovascular disease: Assessing the data from Framingham to the Veterans Affairs High-Density Lipoprotein Intervention Trial. The American journal of cardiology,
86.12 (2000): 19-22.
16. De Oliveira et al. Alcohol consumption raises HDL cholesterol levels by increasing the transport rate of apolipoproteins AI and A-II. Circulation 102.19 (2000): 2347-2352. doi: 10.1161/01.CIR.102.19.2347
17. Van der Gaag M. S., Van Tol A., Vermunt S. H. F., Scheek L. M., Schaafsma G., & Hendriks H. F. J. (2001). Alcohol consumption stimulates early steps in reverse cholesterol transport. Journal of lipid research, 42(12), 2077-2083.
18. Van de Wiel, Albert. The effect of alcohol on postprandial and fasting triglycerides. International journal of vascular medicine 2012 (2011).
19. Nordestgaard B. G., Benn M., Schnohr P., & Tybjærg-Hansen A. (2007). Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA: the journal of the American Medical Association, 298(3), 299-308.
20. Baer, David J. et al. Moderate alcohol consumption lowers risk factors for cardiovascular disease in postmenopausal women fed a controlled diet. The American journal of clinical nutrition 75.3 (2002): 593-599.
21. Whitfield J. B., Heath A. C., Madden P. A., Pergadia M. L., Montgomery G. W., & Martin N. G. (2012). Metabolic and Biochemical Effects of Low‐to‐Moderate Alcohol Consumption. Alcoholism: Clinical and Experimental Research. doi: 10.1111/acer.12015
22. Liu W., Redmond E. M., Morrow D., & Cullen J. P. (2011). Differential effects of daily-moderate versus weekend-binge alcohol consumption on atherosclerotic plaque development in mice. Atherosclerosis, 219(2), 448-454.
23. Pal, S., Ho, N., Santos, C., Dubois, P., Mamo, J., Croft, K., & Allister, E. (2003). Red wine polyphenolics increase LDL receptor expression and activity and suppress the secretion of ApoB100 from human HepG2 cells. The Journal of nutrition, 133(3), 700-706.
24. Lacoste, Lucie, Joseph Hung, and Jules YT Lam. Acute and delayed antithrombotic effects of alcohol in humans. The American journal of cardiology 87.1 (2001): 82-85.
25. Rantakömi, Sanna H. et al. Alcohol consumption and the risk of stroke among hypertensive and overweight men. Journal of neurology 260.2 (2013): 534-539.
26. Kiviniemi Tuomas O. et al. High dose of red wine elicits enhanced inhibition of fibrinolysis. European Journal of Cardiovascular Prevention & Rehabilitation 16.2 (2009): 161-163.
27. Zimmermann, A. J., & Conen, D. (2012). How Does Alcohol Intake Relate to the Risk of Atrial Fibrillation?. JAFIB: Journal of Atrial Fibrillation, 5(4).
28. Ahmed, S. Sultan, and Timothy J. Regan. Heart muscle diseases. The Cardiomyopathies Part III. Cardiotoxicity of alcoholism. Pakistan Heart Journal 14.3 (2012).
29. Gunji Toshiaki et al. Light and moderate alcohol consumption significantly reduces the prevalence of fatty liver in the Japanese male population. The American Journal of Gastroenterology 104.9 (2009): 2189-2195.
30. Dunn, Winston, Ronghui Xu, and Jeffrey B. Schwimmer. Modest wine drinking and decreased prevalence of suspected nonalcoholic fatty liver disease. Hepatology 47.6 (2008): 1947-1954.
31. Liangpunsakul Suthat, and Naga Chalasani. What Should We Recommend to Our Patients with NAFLD Regarding Alcohol. The American journal of gastroenterology 107.7 (2012): 976-978.
32. Tynjälä Joanna et al. Effect of age and gender on the relationship between alcohol consumption and serum GGT: time to recalibrate goals for normal ranges. Alcohol and alcoholism 47.5 (2012): 558-562.
33. Nelson, David E. et al. Alcohol-attributable cancer deaths and years of potential life lost in the United States. American journal of public health 103.4 (2013): 641-648.
34. Bagnardi V. et al. Light alcohol drinking and cancer: A meta-analysis. Annals of oncology 24.2 (2013): 301-308.
35. Boffetta Paolo, and Mia Hashibe. Alcohol and cancer. The lancet oncology 7.2 (2006): 149-156.
36. Laffoy, M. et al. Cancer Incidence and Mortality due to Alcohol: An Analysis of 10-Year Data. Irish (2013): 294.
37. Guénel, Pascal et al. Alcohol drinking may increase risk of breast cancer in men: A European population-based case-control study. Cancer Causes & Control 15.6 (2004): 571-580.
38. Roerecke Michael, and Jürgen Rehm. The cardioprotective association of average alcohol consumption and ischaemic heart disease: A systematic review and meta‐analysis. Addiction 107.7 (2012): 1246-1260. doi: 10.1111/j.1360-0443.2012.03780.x
39. Babor Thomas F. et al. Talk is cheap: measuring drinking outcomes in clinical trials. Journal of Studies on Alcohol and Drugs 61.1 (2000): 55.
40. Di Castelnuovo A., Costanzo S., Bagnardi V., Donati M.B., Iacoviello L., de Gaetano G. Alcohol dosing and total mortality in men and women: An updated meta-analysis of 34 prospective studies. Archives of Internal Medicine. 2006;166: 2437–2445.
41. Fillmore K. M., Kerr W. C., Stockwell T., Chikritzhs T., & Bostrom A. (2006). Moderate alcohol use and reduced mortality risk: Systematic error in prospective studies. Addiction Research & Theory, 14(2), pag. 101-132. doi:10.1080/16066350500497983.
42. Kloner Robert A., and Shereif H. Rezkalla. To drink or not to drink? That is the question. Circulation, 116.11(2007):1306-1317. doi:10.1161/CIRCULATIONAHA.106.678375.
43. Ruidavets Jean-Bernard et al. Patterns of alcohol consumption and ischaemic heart disease in culturally divergent countries: the Prospective Epidemiological Study of Myocardial Infarction (PRIME). BMJ: British Medical Journal 341 (2010).

Articolul The French paradox – between theory & practice apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

– So, is Romania’s entry into the EU beneficial or not for Romanian food producers and consumers?

Implementation of the traceability norms’ consequences on Romanian food producers 

According to the Codex Alimentarius Commission 60-2006, traceability defines the ability to track the movement of food from the farm to the plate, in all stages of production, processing, storage and distribution to the final consumer (who buys food for consumption and not for resale).

According to Article 18 of Regulation 178/2002 of the European Parliament, the traceability:

• it is mandatory to be established at all stages of production and processing;
• food producers are required to have systems or procedures by which to register and to be able to put at the disposal of the authorities the required information on both internal and external traceability.

Internal traceability represents food tracking within a single company.

External traceability represents the information that company receives along with a product from suppliers involved in the previous stages of production.

The implementation of an efficient traceability system is useful for ensuring food safety and quality, but there are implementation factors that can be economically harmful for small, local producers, in terms of costs. And according to Regulation 128/2002, the responsibility for food traceability implementation costs and demands rests entirely on food producers.

Small producers, farmers, fishermen or shepherds are not given free training in order to implement an optimal traceability system, which represents an additional cost added to the already higher production price than that payed by the big producers.

In addition, total trade liberalisation in EU member countries (creating the “single market”) determines the possibility of dumping prices either by multinational corporations with high financial power or by companies in rich countries – where:

• agriculture is subsidised
• the level of automatisation and specialisation of the personnel is more advanced than in poor and middle income countries
• policies regarding the protection of local food producers help them to produce food at a lower price than those in developing countries that just entered this “single market”

Thus, free trade in EU member countries practically suppresses the development of local food production because of the much lower production prices and because of the lack of protection of producers with higher production costs (either due to lack or insufficient subsidies for small producers or due to lack of money for the specialisation of the personnel or the optimum endowment of the production units).

Many small, local food producers fail to meet the required food safety and quality standards of traceability, thus they are not able to sell their products either at a competitive price in their own country or in the single market. 

The endowment and training necessary to implement the traceability systems limit the access of small producers to the single market, pushing them towards bankruptcy in the face of dumping or monopoly policies of large companies or the state.

However, according to the “Declaration on World Food Security” FAO/WHO/1996, the legal definition given to food security does not include the right to food or access to productive resources, but only “access to food”.

Thus, the state does not assume legal obligations or mechanisms to protect the poor or malnourished from the rich, which can hinder their access to productive resources. From a legal point of view, the state is not responsible neither for the hunger, undernutrition or malnutrition of the population nor for the welfare of the local producers.

And the economic inequity between the highly developed and developing EU countries, as well as the social polarisation in our own country, increase both the financial vulnerability of small local producers and the food vulnerability of the poor population.

And, according to the International Planning Committee for Food Sovereignty (2002), “food sovereignty is the right of individuals, communities, populations and countries to define their own policies regarding agriculture, labor, fishing, food and land”.

Sovereignty includes the real right to food and to produce food, and we have almost lost that right because many Romanian food producers cannot afford financially to the big producers in the EU, who can produce and sell more and cheaper on the Romanian market.

In the absence of laws protecting the local food producers, the only alternative of maintaining the right of food sovereignty of the Romanians belongs to the Romanians themselves, by mainly buying the products produced in Romania (optimally, made of ingredients also produced in Romania – which is a second big problem, considering that many large food companies are, in fact, foreign companies that use raw material from other countries, from us using only cheap labor power and nothing else).

In today’s economic context, where free trade rules force the access to foreign products, the promotion of “Made in Romania” foods and the support of agriculture are essential for maintaining Romania’s food sovereignty.

The consequences for the food consumers of the implementation of the Codex Alimentarius rules

The Codex Alimentarius Commission – created by the Food and Agriculture Organization (FAO) and the World Health Organization (WHO) in 1963 under the umbrella of the United Nations – regulates every aspect of production of the food consumed by ± 95% of the world’s population.

The basic official principles of Codex Alimentarius are: consumer protection and fair international trade. Food safety is the central value, the scientific basis emphasised to be extremely solid.

However, the acceptance of the fungicide containing Initium without public consultation (which, according to WHO, is absolutely mandatory) seems to be in a hurry.

On January 11, 2010, Romania joined the Codex Alimentarius Commission (1) and the first duty as a member was to willingly accept to be the first country in the world to use BASF’s new fungicide: Ametoctradin (Initium) (2).

In accordance with Article 8 of Directive 91/414/EEC – regarding the placing on the European market of plant protection products – it is stipulated that an EU Member State may provisionally authorise, for a period not exceeding 3 years, the placing on its own market of plant protection products containing new substances (defined as active substances that are not included in the annex to this directive as being active substances authorised as safe for humans) to gradually evaluate the impact on the population.

By law, active substances that are not known to be safe for human consumption – such as Initium – can be used legally in the production of plants for human consumption, to scientifically evaluate the impact on humans. 

And, although many richer and more “civilised” countries than Romania welcomed our decision, they did not rush to authorise the use of the fungicide with Initium in their own countries.

Here is a question asked by two Romanians to the Commission of the European Parliament on February 22, 2010 (code E-0918/10):

„Written question from Rareş-Lucian Niculescu (PPE) and Elena Oana Antonescu (PPE) to the Commission of the European Parliament:

Subject: Evaluation of fungicide with Initium in accordance with the norms of Directive 91/414/EEC

In January, Romania granted a temporary authorisation for the fungicide containing Initium for a period of three years, in accordance with Article 8 of Directive 91/414/EEC corresponding to the placing on the market of plant protection products. The substance is used for the antifungal protection of grapes and vegetables.

This fungicide was the subject of an evaluation report by the European Food Safety Authority, adopted in October 2009 (“EFSA-Q-2009-00700 – Reasoned opinion of EFSA: Setting of new MRLs for BAS 650 F”) for table or wine grapes, tomatoes, peppers, cucumbers, melons and green salad. Considering the Romanian citizens worried about the possible negative impact that the use of this fungicide could have on health, can the Commission answer the following question:

Given the fact that this evaluation report has not been analysed by other researchers (the peer review procedure) and that the conclusions of the report are considered provisional, what is the current status of this procedure in accordance with Directive 91/414/EEC?

Link to the European Parliament

And here’s the answer from the European Parliament.

Questions in Parliament

Date: March 29, 2010

Code: for question E-0918/10 and P-1123/10

Answer given by Mr Dalli on behalf of the Commission:

“In order to facilitate the placing on the market of new and innovative plant protection substances, Article 8 (1) of Directive 91/414/EEC (1) on the placing of plant protection products on the market allows the possibility of authorizing products containing new active substances for a limited period of three years, if a complete file has been submitted and if the member state authorizing the use of the product sets high safety standards in accordance with Directive 91/414/EEC.

Commission Decision 2009/535/EC (2) recognizes in principle the file submitted by BASF SE to support the inclusion of the substance under the development license ‘BAS 650F’. This substance has the ISO name of ‘ametoctradin’ and the registered trademark ‘Initium’. Therefore, any member state may provisionally authorize the use of products containing this substance.

When authorizing a plant protection product, a member state must assess whether the high standards of human and animal safety and those of environmental protection under European law are met for all types of guaranteed use. Granting the provisional authorization is no exception to this rule, so safety standards are not compromised. When granting the temporary authorization, the member state decides to undertake the entire risk assessment on its ownand, therefore, not to fully benefit from the peer review procedure. However, in doing so, the member state may accelerate the entry into the market of innovative products, which may be safer for consumers and the environment compared to other products.

The Commission intends to adopt temporary maximum doses (MRLs) (3) for ametroctatid (Initium) based on EFSA’s substantive opinion of October 2009 (4). The proposed MRLs are provisional due to the lack of completion of the peer review procedure, being based on the information evaluation from the temporary evaluation of the ametoctradin report. Both reports are produced by the Netherlands, which conducts the EFSA peer review procedure. The procedure has already been voted by SCFEAH and it is expected to be published in the Official Journal at the latest in the third quarter of 2010“.

Link to the European Parliament

So, despite the fact that Initium’s safety has not been evaluated by other scientists besides those employed by BASF, the product is still used today, years later, legally in about 30 countries, despite the fact that the authorization is only temporary and cannot guarantee the safety of consumption over human health.

All in the name of food safety and of fair trade.

The idea behind the use of a new substance with toxic potential under the provisional authorization of Codex Alimentarius has behind the growing global population and the need to develop biotechnologies that increase productivity in agriculture and the term of guarantee of food products.

It does not seem to matter that the number of children born per woman worldwide dropped from 5.02 to 2.65 between 1950 and 2005 and that this number is expected to drop to 2.05 by 2050 (3).

It also does not seem to matter that the mortality rate is estimated to increase from 56 million per year to 80 million per year (4).

Economists make mathematical, not biological, estimates not taking into account the fact that the fertility rate is declining and that mortality rate gradually will double.

At the global level, the question of the survival of the people living in poor countries is raised, only that the population of these countries seems to have nothing to say about the problem of their own survival.

– These people are not asked about why would they prefer to die: from hunger or from cancer, or from diseases of the reproductive system, autoimmune diseases, endocrine or other neurological dysfunctions?

Big countries decided for them that they must be fed with whatever possible even if the food they are fed with might make them ill.

All of these are side effects of possible exposure to fungicides and pesticides quoted from the official website of the World Health Organization. WHO also claims that adults are at lower risk than children and that more deaths due to fungicides have been recorded in developing countries (5,6).

The cancer rate of Romanians increased with ± 30%, from 51,450 cases in 2011 to 78,760 cases at the end of 2012 (7). 

And of course no one can associate the use of Initium with this increased cancer incidence.

But, although there is no evidence to link Initium with the 30% increase in cancer rates in the first two years after Initium’s provisional authorization, we cannot deny the coincidence. At least this coincidence should force WHO to consider all possible etiological factors that have caused so many Romanians to develop cancer in such a short time.

If Initium has been provisionally authorized for evaluation, at least the evaluation should be done.

However, despite the fact that years have passed since the provisional authorization to evaluate the effects on humans, searching for the keywords ‘Initium’ or ‘Ametoctradin’ does not get any results neither on the official website of Codex Alimentarius, nor on the one to WHO (8). All we can get, if we insist on the searches, is the Official Opinion, without the peer review procedure (which has not yet been done, although many more than the initial 3 years have passed since the provisional authorization), published in the EFSA Journal in 2009.

– Is it sufficient for the food security of Romanians?

– Is it sufficient for the health of the people in the 30 countries that continue to provisionally authorize the use of Initium?

– Given the harmful impact, shouldn’t potentially toxic substances be tested and pre-approved as safe by other scientists other than those paid by the manufacturers of these substances themselves? (9)

– And is the legal pre-authorization of a potentially dangerous substance without the peer review procedure for the benefit of the people?

– What’s the rush?!

On the WHO website, there are a number of protocols and warnings regarding the toxicity of pesticides and fungicides on both human health and the environment. Thus, countless fungicides and pesticides provisionally authorized have been shown to induce cancer and infertility (10-13).

– Isn’t this proof that the provisional approval procedure is in fact the legal acceptance to use people as lab rats?

– And how can scientists determine if the maximum permissible doses for human safety have a protective effect, considering that the actual quantitative consumption of plants by various people cannot be estimated?

– And shouldn’t there have been a public debate prior to the granting of the Initium temporary authorization?

Because the legal use of Initium has not been discussed in the media, announced or debated except in the corners, most Romanians could consume over the amount for which the maximum provisional doses allowed for Initium were calculated – from basic products such as bread, pasta and other bakery products, cucumbers, tomatoes, onions, potatoes, grapes, melons, green salad.

However, although it seems that we were used as laboratory mice (with the agreement of the Romanian authorities of course), in Romania we still have access to tomatoes that taste like tomatoes and to strawberries that do not taste like cucumbers.

We can still buy eggs from chickens raised in the back yard and milk from small local producers.

We still cook at home…

The entry of Romania into the civilised world of the European Union and into the Codex Alimentarius universe had a powerful impact:

• on local food producers, many failing due to the inability to provide the standards and norms in force at competitive prices, not even on the local market,
• on food consumers, many cannot avoid the consumption of food of plant origin enhanced with new substances such as Initium, substances not yet proven to be safe for human consumption.

Romanian legislation by which local producers and Romanian consumers should be protected should really protect us, not just allow others to use us as a market for sales and as lab rats, behind the pink idea fair trade for all.

But, unfortunately, someone has to pay the salaries of scientists.

The reason that moves science is not charity, but profit. And we, the Romanian consumers and producers, are not so rich as to attract the attention of the big international corporations.

The studies are done on us.

But they are done to justify the use of these “new innovative substances” in countries with much greater financial power (14).

Maybe that’s why we still rank only 10th in the top of European countries with the most cancer patients.

Maybe that’s one of the why the big, modern, civilised countries are at the top of cancer incidence.

These tests are not for us.

Quoted studies

1: Taylor, Paul Anthony. Codex Guidelines for Vitamins and Minerals – Optional or Mandatory? Dr. Rath Health Foundation. http://www4.dr-rath-foundation.org/features/codex_wto.html.

2: World Resources Institute. Earthtrends.wri.org. Retrieved 2011-11-30.

3: World Population estimates by the US Census Bureau. USCB. Retrieved May 22, 2012.

4: http://www.who.int/bulletin/volumes/82/11/editorial31104html/en/

5: http://www.who.int/mediacentre/news/notes/2004/np19/en/

6: Ferlay, J., et al. Cancer incidence and mortality patterns in Europe: Estimates for 40 countries in 2012. European Journal of Cancer (2013). International Agency for Research on Cancer, http://eco.iarc.fr/eucan/Country.aspx?ISOCountryCd=642.

7: http://www.codexalimentarius.org; http://www.who.org.

8: http://www.efsa.europa.eu/en/efsajournal/doc/1367.pdf

9: Cantelli-Forti, G., M. Paolini, and P. Hrelia. Multiple end point procedure to evaluate risk from pesticides. Environmental health perspectives 101.Suppl 3 (1993): 15.

10: Hrelia, P. et al. Cytogenetic effects of Metalaxyl on human and animal chromosomes. Mutation Research/Genetic Toxicology 369.1 (1996): 81-86. doi: 10.1016/S0165-1218(96)90051-8.

11: Poli, P. et al. Evaluation of the genotoxicity induced by the fungicide fenarimol in mammalian and plant cells by use of the single-cell gel electrophoresis assay. Mutation Research/Genetic Toxicology and Environmental Mutagenesis540.1 (2003): 57-66. doi: 10.1016/S1383-5718(03)00165-7.

12: Hrelia, P., Fimognari, C., Maffei, F., Vigagni, F., Mesirca, R., Pozzetti, L., … & Forti, G. C. (1996). The genetic and non-genetic toxicity of the fungicide Vinclozolin. Mutagenesis, 11(5), 445-453. doi: 10.1093/mutage/11.5.445.

13: Fan, WuQiang et al. Atrazine-induced aromatase expression is SF-1 dependent: implications for endocrine disruption in wildlife and reproductive cancers in humans. Environmental Health Perspectives 115.5 (2007): 720.

14: BASF sells INITIUM® products in 11 European countries and obtained authorizations in 28 countries worldwide. BASF press release: http://www.basf.com/group/pressemitteilungen/P-10-110.

Articolul Made in Romania apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Now, most adults recognise the signs of dehydration and take them seriously when it comes to their own children.

We know that a child with obvious signs of advanced dehydration – pale skin, burning lips, fatigue or apathy, superficial breathing, cramps, nausea and confusion – should be consulted urgently by a doctor who may prescribe rehydration salts and diet or even hospitalisation. For example, such dehydration can occur in an enterocolitis episode, when diarrhea, vomiting or fever, abdominal colic, chills and nausea occur after eating a contaminated food. However, some of the parents of these children use dehydration for weight loss, forcing them to ignore how they feel when they experience the same symptoms of dehydration. Everything in the name of fast weight loss.

The first bad news is that the fat tissue mostly contains no water. 

If you retain water, you don’t care if the fat tissue contains water or not: you see that today you do not fit to your yesterday pants, and you feel like screaming at the mirror.

But dehydration as a weight loss solution will make you retain even more water in the long term and it will overstimulate the hunger centre from your hypothalamus. Practically, it will be harder and harder for you not to eat whenever, because you will be hungry more often. Then your hunger will increase in parallel with your fat percentage. And it will not increase for foods high in protein (which could help you with your water retention and fat loss), but for foods high in fat and sugars.

The second bad news is that although supplements that “eliminate water retention” are cheap and effective in the short term, legally they don’t need to be tested in the long term. 

The difference between drugs and supplements is not that supplements have no side effects but that they legally must not be tested the same as drugs. Although a cheap + fast results product is a safe recipe for success, these products are not as pink as we would like them to be.

I’ve heard so many times, “Take this, it’s natural / it’s only herbs, do not worry” that sometimes I wonder if pharmacists or various specialists recommending dietary supplements know the legislation behind these products. Cocaine is natural too.

The fact that many people chose not to not look behind the nice pink fence painted by food supplements manufacturers does not mean that these products have no side effects.

In order to better understand what I mean, I will use 3 purely natural supplements – zinc, cranberry and nettle extract – which are “completely pink” on the paper, but contain active substances that can interact with other active substances (either exogenous from other supplements or drugs administered in parallel, or endogenous – involved in various processes of your body).

Zinc supplements interfere with:

• the efficacy and side effects of anticoagulant medications and supplements (heparin, Ginkgo Biloba), non-steroidal anti-inflammatory drugs (aspirin, ibuprofen), hypoglycemic drugs (insulin or other drugs for diabetes), antibiotics, antidiarrheals, antidepressants and many others
• the intestinal absorption of iron, calcium, magnesium, phosphorus, vitamins B, A and D.

Some effects appear more frequently epidemiologically, others are only demonstrated in the laboratory. And we can ignore them comfortably because they are not mentioned on the tag.

Cranberries  are delicious and I highly recommend them: along with a bunch of raw almonds, for example, they can provide a healthy meal when you have no time or access to other foods.

But the daily intake of cranberries supplements can cause abdominal cramps and diarrhea or can mask an insufficiently treated urine infection, no matter if they were taken for water retention or for urinary infection.

Also, because they contain large amounts of oxalate, excessive intake may increase the risk of urinary lithiasis, further increasing the risk of urinary infection.

And, just like zinc, cranberry supplements may increase the risk of bleeding, especially in people taking anticoagulant drugs like Aspenter, because of the high salicylic acid content (yes, exactly, aspirin).

The keyword in this story is “excessive” – word whose practical significance varies from one person to another, and – in the same person – depending on the state of health and the co-intake of other drugs or supplements.

Nettle – has been on the market “since grandmother was young” and we eat it with great pleasure during spring in soups or mashed with egg and polenta. Everybody knows it is healthy, and I do not say otherwise. Just one thing is to eat or drink some tea from time to time, and another thing is to take supplements containing nettle extract. But, as many times happens, more of a good thing is not necessarily better.

Excessive intake of nettle dietary supplements can cause abdominal cramps, abundant sweating, diarrhea, and they interfere with anti-diabetic, anticoagulant, antihypertensive or anti-inflammatory medication.

This does not mean that – occasionally administered – zinc, cranberry or nettle extract would be dangerous, but that the same risk / benefit ratio that you do mentally when deciding whether or not to take a drug should also be done when deciding whether or not to take a dietary supplement.

The third bad news is that the retention of water per se may worsen as you use drugs or supplements for water retention. 

Even the most natural diuretics do not treat the cause of water retention, but the effect. If you retain water, you first need to know why you’re retaining water.

Water retention may have a behavioural cause. And, although it occurs in people standing too much, it also occurs in those who sit for hours in the office: after long days many feet swell and tend to get out of their shoes and many rings are moved on smaller fingers.

In addition to office sedentariness, the extra 2 kg that appear every evening in the body of many people who retain water is also due to the on-the-run intake of foods or drinks too rich in salt (fast food, pizza, pickles, canned food, sausages and other deli meats). And then they are only hydrating with coffee, tea and soft drinks – and not with water, because… they retain the water.

Moreover, too drastic diets packed with periodic overeating – and again diets, and again overeating – may even worsen water retention. And so, day by day, until you no longer recognise your body in the mirror.

So – before you take more or less natural diuretics – please think if:

1. is there a medical cause behind your water retention?
2. do you also take other dieteray supplements or medications?
3. do you do sports?
4. are your abdomen and thighs toned enough to wear those high heels?
5. do you eat on-the-run foods high in salt?
6. do you constantly hydrate only with soft drinks and coffee?
7. do you go on drastic diets and then overeat?

Still treating the effect by ignoring the cause will only aggravate that cause.

Articolul 7 essential questions if you have water retention apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

I’ll explain Top 3 factors that contribute to weight gain during holiday.

First of all, I would like to point out that yes, you have read correctly: there are some factors that make you gain weight on holiday, not the food itself.

And yes, I know that chocolate has saturated fats and that pizza or Sicilian pasta have a glycemic index as high as the Trajan’s Column. Still, the bio avocado fattens as much as the most delicious tart if you eat it mindlessly.

So let me explain to you how the conjuncture factors – and not the food itself – fatten you every time, whether it is an ultra all inclusive holiday in Antalya, a city break in Rome or a Christmas in Vienna.

Then I’ll introduce 3 effective solutions that, when properly applied every day, prevent fattening on holiday because it solves these 3 factors just before you actually go on holiday.

Now, before I begin, I would like to mention that if you are 30 years old, you have a lot of abdominal fat, you work from morning till night, you eat all kinds of nonsense food and you are on the verge of depression, probably by applying these 3 solutions, your life and body image will only begin to improve if you’ll start using the information below.

Your metabolism is low, you probably have insulin resistance, disturbed appetite, and dopaminergic receptors in free fall.

It happens.

But the only difference between you and better you is YOU.

So, if you do not apply these 3 solutions at least now, that you are home, without a world of culinary temptations, then we are wasting time together.

And probably this article will not help you because the unapplied information has zero value.

But if you’re tired of keeping infinite diets and then getting more weight with each holiday, then apply the solutions every day for 21 days (yes, just as you know it takes you to form a new reflex). You’ll be delighted with the result!

So, here are the main factors that make you gain weight on holiday:

1. diversity
2. uncertainty
3. legitimacy

Most of us are overcome when we see a sea of food, which looks beautiful, fresh and smells heavenly. It is absolutely normal! As normal as the fact that most men marry beautiful women dressed in white.

Solution no. 1 so you do not get fat on holiday is: THE MOTHER-IN-LAW.

Yeah, you read correctly – and I do not ask you to take her with you on the holiday, but to behave as if you were the mother of one of those men who had entered the blind week, a real mother-in-law, with super airs and whims.

Basically, before you eat anything, you have to choose 2-3 foods you would give an absolute 10 out of 10 for wearing, showing and make-up. Maximum artistic impression!

In order not to get fat on holiday or on Christmas or visiting or elsewhere you’ll face food mountains, you have to have super airs and whims, and act more pretentious than a mother-in-law.

So choose only those dishes you really like and enjoy each piece with the greatest excitement, without fear or regret.

Solution no. 2 so that you do not get fat on holiday is: YOUR RIGHT FIST.

Most girls’ fathers have two fears:

1. That their girl will find someone and get married.
2. That their girl will not find someone and get married.

So is eating on holiday:

1. what do you do if the food is delicious?
2. what do you do if the food is not delicious?

No matter how good or bad is food on holiday, so as not to get fat on that holiday, you have to face this dilemma with determination.

So, you apply the mother-in-law method and choose 2-3 of the best dishes available, savour piece by piece and promise to eat at the next table other 2-3 dishes of the ones that tempted you.

Seriously: 2-3, not more, as your stomach is not a car trunk. If you want to not gain weight during the holiday, the food you put in there should not push your liver for more room inside your abdomen.

Your fasting stomach has ~ the size of the right fist and. So, to feel the optimal moment of satiety, no meal should exceed 2-3 portions, each of the size of your right fist.

Solution no. 3 so that you do not get fat on holiday is: YOUR HUNGER SENSATION.

It is your right to to eat the most delicious meals.

It is perfectly legitimate!

I do it when I’m not on vacation, absolutely every day.

Just that nibbling mindlessly on this or that when you are not hungry gets you fattened on whatever you eat, be it healthy nuts or fried potato chips.

It does not matter how little calories you consume, what glycemic index, what glycemic load or how you combine the foods. If you are not hungry and nibble: bye, bye silhouette.

You can perceive hunger at the head of the chest, with the same degree of intensity as pee feeling, that is:

• 0 if you do not need to eat,
• 1 if you feel like eating, but you can still wait, and
• 2 if you are just as hungry how hard are you to pee.

So, to not to get fat on your lovely holiday:

1. be pretentious as a mother-in-law
2. think like bride’s father and
3. go to the bathroom before you wet your pants.

1. eat only foods that you’d grade a 10 out of 10
2. limit yourself to 2-3 dishes, each of the size of your right fist,
3. wait for you to get hungry before you eat anything.

Applying these 3 solutions, you will not gain weight in any holiday in your life, but you can even slim while you are on holiday. All you have to do is apply them consistently.

To  our health!

Articolul Top 3 factors that contribute to holiday weight gain & what to do about them apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.