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.

And I wrote “sadly” for two reasons:

1) Because putting the equal sign between health and alkalinity ignores the fact that anyone can instantly become alkaline when they:

• vomit (Mehler & Walsh, 2016)
• have a thermal shock in case of heat stress (Bain et al., 2015)
• have fever (Schuchmann et al., 2011)
• have a stroke (Zöllner et al., 2015)

2) Because the target audience of alkaline water and water alkalizing devices are often cancer patients.

Just that the story about improved health through modifying pH either by alkaline diet either by drinking alkaline water is quite hype.

We know from a long time now that malignant cells that use the Warburg effect (aerobic glycolysis) have an alkaline intracellular pH and an acidic extracellular one – alkalinity helping them to avoid apoptosis, to proliferate and to metastasise (Griffiths, 1991; Harguindey et al., 2005; White et al., 2017).

Some preclinical studies performed on glycolytic malignant cellular lines or on mice with homogeneous glycolytic malignant tumours show that extracellular alkalinity could contribute to destroying these types of malignant cells (Mazzio et al., 2012; Yustisia et al., 2017). Other studies confirm this conclusion, but also show that in the case of malignant cells that do not use the Warburg effect alkalizing the extracellular environment can help them proliferate and metastasise (Wanandi et al., 2017).

The attempt to counteract extracellular acidosis induced by aerobic glycolysis by drinking alkaline water ignores the fact that in vivo tumours are heterogeneous and that malignant cells are highly adaptive (Vlashi et al., 2014; Xie et al., 2014; Obre & Rossignol, 2015) as they can survive by using other metabolic pathways than aerobic glycolysis: the Crabtree effect, (Jones & Thompson, 2009) the reverse Warburg effect (Pavlides et al, 2009), entosis (Lozupone & Fais, 2015) etc.

And a metabolic analysis performed on 740 biopsies from breast cancer patients shows that only 40.3% of the studied tissue samples presented aerobic glycolysis (Choi et al, 2013). We wipe out the fact that even in tumours with the same localisation we cannot simply tell by default that drinking alkaline water associate apoptosis or malignant proliferation and metastasis, we wipe out the fact that 60 is bigger than 40 and we sell assumptions to confuse and desperate patients.

Besides many mammary malignant cells, also many ovarian cancer cells and prostate cancer cells prefer to use the reverse Warburg effect, the Crabtree effect, entosis or autophagy (Whitaker-Menezes et al., 2011; Schlaepfer et al., 2014; Nieman et al., 2011).

We have no randomised controlled study performed on cancer patients treated with intention to cure to prove that alkaline water contributes to healing cancer or that it prevents this diagnosis – researchers considering that promoting alkaline water is scientifically unjustified in oncological context (Fenton & Huang, 2016).

There is only marketing based on studies performed on cell lines and on laboratory animals that support hypotheses outside the complex malignant metabolic context of heterogeneous tumours developed in vivo in humans.

Of course, anyone can spend their money on whatever they want as most people haven’t enough patience to develop heat shock or a stroke to become more alkaline. Not even in August.

References

Bain AR et al. “Cerebral vascular control and metabolism in heat stress.”Comprehensive Physiology (2015).

Choi J et al. “Metabolic interaction between cancer cells and stromal cells according to breast cancer molecular subtype.” Breast cancer research15.5 (2013): R78.

Fenton TR & Huang T. “Systematic review of the association between dietary acid load, alkaline water and cancer.”BMJ open 6.6 (2016): e010438.

Griffiths JR. “Are cancer cells acidic?” British journal of cancer 64.3 (1991): 425.

Harguindey S et al. “The role of pH dynamics and the Na+/H+ antiporter in the etiopathogenesis and treatment of cancer. Two faces of the same coin—one single nature.” Biochimica et Biophysica Acta (BBA)-Reviews on Cancer1756.1 (2005): 1-24.

Heil DP. “Acid-base balance and hydration status following consumption of mineral-based alkaline bottled water.” J Int Soc Sports Nutr 7.1 (2010): 29.

Jones RG & Thompson CB, 2009. Tumor suppressors and cell metabolism: A recipe for cancer growth. Genes & development, 23(5), 537-548.

Lozupone F & Fais S, 2015. Cancer Cell Cannibalism: A Primeval Option to Survive. Current molecular medicine, 15(9), 836-841.

Mehler PS & Walsh K. “Electrolyte and acid‐base abnormalities associated with purging behaviors.” International Journal of Eating Disorders (2016).

Nieman KM et al. Adipocytes promote ovarian cancer metastasis and provide energy for rapid tumor growth. Nature medicine. 2011;17(11):1498-503.

Obre E & Rossignol R. Emerging concepts in bioenergetics and cancer research: metabolic flexibility, coupling, symbiosis, switch, oxidative tumors, metabolic remodeling, signaling and bioenergetic therapy. The international journal of biochemistry & cell biology. 2015; 59:167-81.

Pavlides S et al, 2009. The reverse Warburg effect: aerobic glycolysis in cancer associated fibroblasts and the tumor stroma. Cell cycle, 8(23), 3984-4001.

Schlaepfer IR et al. Lipid catabolism via CPT1 as a therapeutic target for prostate cancer. Molecular cancer therapeutics. 2014;13(10):2361-71.

Schuchmann S et al. “Respiratory alkalosis in children with febrile seizures.” Epilepsia 52.11 (2011): 1949-1955.

Vlashi E et al. “Metabolic differences in breast cancer stem cells and differentiated progeny.” Breast cancer research and treatment 146.3 (2014): 525-534.

Wanandi SI et al. “Impact of extracellular alkalinization on the survival of human CD24-/CD44+ breast cancer stem cells associated with cellular metabolic shifts.” Brazilian Journal of Medical and Biological Research 50.8 (2017).

White, KA et al. “Cancer cell behaviors mediated by dysregulated pH dynamics at a glance.” J Cell Sci 130.4 (2017): 663-669.

Whitaker-Menezes, Diana, et al. “Hyperactivation of oxidative mitochondrial metabolism in epithelial cancer cells in situ: visualizing the therapeutic effects of metformin in tumor tissue.” Cell cycle 10.23 (2011): 4047-4064.

Xie J et al. “Beyond Warburg effect–dual metabolic nature of cancer cells.” Scientific reports 4 (2014): 4927.

Yustisia I et al. “Effects of extracellular modulation through hypoxia on the glucose metabolism of human breast cancer stem cells.” Journal of Physics: Conference Series. Vol. 884. No. 1. IOP Publishing, 2017.

Zöllner JP et al. “Changes of pH and Energy State in Subacute Human Ischemia Assessed by Multinuclear Magnetic Resonance Spectroscopy.” Stroke 46.2 (2015): 441-446.

Articolul Alkaline water and cancer 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.

Among other side effects reported by patients during antiestrogenic treatment, the main complain is muscle and joint pain. And among other side effects reported by patients during statins treatment, the main complain is also muscle and joint pain. So – at least because of this shared side effect that can be co-amplified when both treatments are administrated simultaneously – we should first ask the question:

– Can ER+ breast cancer patients take statins during antiestrogenic treatment?

But first, let`s start with a far more important question:

– Can breast cancer patients take statins?

Of course, anyone can take a pill – the second question refering to statins’ carcinogenity and long term safety when administred to breast cancer patients and not to the kinetic ability to swallow a pill.

Epidemiological studies state that statins administration does not increase the risk of cancer – Browning si Martin, 2007. But we don’t have randomised controlled trials that prove statins safety for breast cancer patients.

All we have is a multitude of epidemiological studies with head-to-head contradictory results:

– statins administration in people without cancer:

• is not associated with increased risk of breast cancer – Cauley et al., 2006
• is not associated with decreased risk of breast cancer –  Undela, Srikanth and Bansal, 2012
• is associated with increased risk of breast cancer – McDougall et al., 2013
• is associated with decreased risk of triple negative breast cancer – Kumar et al., 2008
• is not associated with decreased risk of triple negative breast cancer – Woditschka et al., 2010

– statins administration in breast cancer patients:

• is associated with a decreased risk of recurrence – Kwan et al., 2008
• is not associated with a decreased risk of recurrence – Nickels et al., 2013
• is associated with a decreased risk of breast cancer mortality – Murtola et al., 2014
• is not associated with a decreased risk of breast cancer mortality – Smith et al., 2016

Despite these contradictory results, one of the systematic reviews of the epidemiological studies on breast cancer and statins connection concluded that statins administration appears to be safe and potentially beneficial for breast cancer patients  (Manthravadi, Shrestha si Madhusudhana, 2016).

So, one: Epidemiological studies – in English, studies that do not prove causality but just raise questions about possible risk factors that should be further tested in randomised controlled trials – claim that statins seem to be safe from an oncological point of view when administered to breast cancer patients, even though we don’t know if this epidemiological hypothesis is true or not.

But – even though statins are among the most sold medications on the planet – paradoxically, the systematic review don by Ravnskov et al. in 2016 shows that people over 60 years of age with high LDL-cholesterol levels leave as much or more than people with low LDL-cholesterol levels.

So, two: The fact that lowering cholesterol by administering statins has a beneficial clinical impact is a generalization not a certainty.

And we know that statins administration side effects associate the main sarcopenic obesity causes:

• sarcopenia (gradual loss of muscle mass) – Wilke et al., 2007 ; Prado et al., 2011
• hyperinsulinism and insulin resistance – Goldstein and Mascitelli, 2013; Aiman, Najmi and Khan, 2014

So, three: Statins administration to breast cancer patients can indirectly increase the risk of obesity.

And breast cancer patients’ obesity increases the risks of metastasis, recurrence and mortality.

References

Aiman, U., Najmi, A., & Khan, R. A. (2014). Statin induced diabetes and its clinical implications. Journal of pharmacology & pharmacotherapeutics, 5(3), 181.

Browning, D. R., & Martin, R. M. (2007). Statins and risk of cancer: a systematic review and metaanalysis. International journal of cancer, 120(4), 833-843.

Cauley, Jane A., et al. “Statin use and breast cancer: prospective results from the Women’s Health Initiative.” Journal of the National Cancer Institute 98.10 (2006): 700-707.

Goldstein, M. R., & Mascitelli, L. (2013). Do statins cause diabetes?. Current diabetes reports, 13(3), 381-390.

Kumar, Anjali S., et al. “Estrogen Receptor–Negative Breast Cancer Is Less Likely to Arise among Lipophilic Statin Users.” Cancer Epidemiology and Prevention Biomarkers 17.5 (2008): 1028-1033.

Manthravadi, S., Shrestha, A., & Madhusudhana, S. (2016). Impact of statin use on cancer recurrence and mortality in breast cancer: A systematic review and meta‐analysis. International journal of cancer, 139(6), 1281-1288.

McDougall, J.A., Malone, K.E., Daling, J.R., Cushing-Haugen, K.L., Porter, P.L. and Li, C.I. (2013) Long-Term Statin Use and Risk of Ductal and Lobular Breast Cancer among Women 55 to 74 Years of Age. Cancer Epidemiology, Biomarkers & Prevention, 22, 1529-1537.

Murtola, Teemu J., et al. “Statin use and breast cancer survival: a nationwide cohort study from Finland.” PloS one 9.10 (2014): e110231.

Nickels, Stefan, et al. “Mortality and recurrence risk in relation to the use of lipid-lowering drugs in a prospective breast cancer patient cohort.” PloS one 8.9 (2013): e75088.

Prado, Carla MM, et al. “Two faces of drug therapy in cancer: drug-related lean tissue loss and its adverse consequences to survival and toxicity.” Current Opinion in Clinical Nutrition & Metabolic Care14.3 (2011): 250-254.

Ravnskov, Uffe, et al. “Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review.” BMJ open 6.6 (2016): e010401.

Smith, Amelia, et al. “De novo post-diagnosis statin use, breast cancer-specific and overall mortality in women with stage I-III breast cancer.” (2016): 592.

Undela, Krishna, Vallakatla Srikanth, and Dipika Bansal. “Statin use and risk of breast cancer: a meta-analysis of observational studies.” Breast cancer research and treatment 135.1 (2012): 261-269.

Wilke, R.A., Lin, D.W., Roden, D.M., Watkins, P.B., Flockhart, D., Zineh, I., Giacomini, K.M. and Krauss, R.M. (2007) Identifying Genetic Risk Factors for Serious Adverse Drug Reactions: Current Progress and Challenges. Nature S. Moonindranath, H. L. Shen 29 Reviews: Drug Discovery, 6, 904-916

Woditschka, Stephan, et al. “Lipophilic statin use and risk of breast cancer subtypes.” Cancer Epidemiology and Prevention Biomarkers(2010): cebp-0524.

Articolul Can breast cancer patients take statins? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Although the word „cancer“ covers a multitude of localisations, loco-regional or distance disorders, immunohistochemistry and genetic mutations – and therefore completely different evolutions and treatments from one patient to another, even for patients with the same localisation – pseudo-oncology sells all sorts of panacea good for any type of cancer one might have.

We do not know what happens long-term to the patient who is using complementary-integrative “medicine” because these systems are not legally required to monitor patients long-term. By law, such pseudo-oncology products and strategies can be sold based on the supposition that they are safe. The safety is not tested or addressed in any way, it is assumed.

– Still, can we put the equal sign between tumour disappearance and cancer cure?

Scientifically, the disappearance of the tumour is called “complete pathological response” – and in allopathic medicine can be obtained surgically or by chemotherapy.

The hypothesis that tumour disappearance means cancer cure has been contradicted for decades by the fact that the surgical removal of the tumour does not necessarily mean that the cancer is cured (Haagensen et al., 1951).

Also, if surgical removal of cancer does not necessarily mean healing, the same is true sometimes in the case of tumour disappearance by chemotherapy (Cortazar et al., 2014).

For example, we know that patients with triple-negative breast cancer or HER2+ often respond very well to chemotherapy given immediately after diagnosis, obtaining tumor disappearance before surgery (therapeutic response called “pathologic complete response”), and that such response can sometimes be obtained even in multicenter tumours (Ataseven et al., 2015).

And according to the current scientific data we also know that the surgical intervention remains important even after obtaining pathologic complete response to neoadjuvant chemotherapy. (Ring et al., 2003; Clouth et al., 2007; Daveau et al., 2011).

So, the complete disappearance of the tumour does not mean curing cancer, we know that for a long time, and we do not hide under the carpet that we know.

The honest treatment efficiency evaluation is the essential difference between complementary-integrative “medicine” and allopathic medicine.

In spite of the various personal examples quoted and promoted as proof that you can naturally cure your own cancer without oncological treatment, based on the available scientific data:

• the ketogenic diet is not recommended for any patient with cancer diagnosis (Erickson et al., 2017)
• administration of various dietary supplements during chemotherapy is associated with decreased survival (Smith et al., 2016)
• vitamin C administration does not have antitumoral effect, even at huge doses of 70, 90 or 110 g/m2 administered intravenously (Hooffer et al., 2008)
• antioxidants administration during oncological treatment is contraindicated (Seifield et al., 2003)
• antioxidants may increase the metastasis risk (Herraiz et al., 2016)

Unlike complementary-integrative medicine, oncology is based on the objective treatment efficiency evaluation:

• in the short-term – the periodic evaluation of the pathological response is essential for each patient’s treatment individualisation
• in the long-term – the regular clinical and imagistic evaluation are essential for the early diagnosis of any possible metastasis or recurrence that might occur after treatment even in the case of patients that actually obtained pathologic complete response

So, if you are an oncological patient and you are tempted to try a “miracle” that “cured” another person’s cancer “naturally”, ask yourself at least these three questions:

1. Has the cured cancer been objectively evaluated in an imagistic, histopathological or clinical way? Or the disappearance of the tumour is simply assumed based on the fact that the patient “feels better”?
2. Compared to you, did the person have the same cancer location, the same type of cancer and the same number of tumours?
3. Compared to you, did the person have the same lymph node or the same metastases?
4. Compared to you, did that person have the same age, same sex and identical family history?
5. Compared to you, did the person suffer from the same diseases other than cancer?
6. Compared to you, did that person gained or lose weight after diagnosis?
7. Do you know what happened to that person after 10, 15 – or at least 5 years?

I know I wrote more than 3 questions. But there are so many differences even between two people with exactly the same immunohistochemical type of cancer that I can still write so many other questions.

Cocaine is also natural and it has side effects.

The tumour disappearance should be monitored long, loong, looong time to be able to say that patient is cured – which is why the clinical and radiological controls that are regularly performed long-term after cancer disappearance are absolutely essential.

Quoted studies

Ataseven, Beyhan, et al. “Impact of multifocal or multicentric disease on surgery and locoregional, distant and overall survival of 6,134 breast cancer patients treated with neoadjuvant chemotherapy.” Annals of surgical oncology 22.4 (2015): 1118-1127.

Clouth, B., et al. “The surgical management of patients who achieve a complete pathological response after primary chemotherapy for locally advanced breast cancer.” European Journal of Surgical Oncology (EJSO) 33.8 (2007): 961-966.

Cortazar, Patricia, et al. “Pathological complete response and long-term clinical benefit in breast cancer: the CTNeoBC pooled analysis.” The Lancet 384.9938 (2014): 164-172.

Daveau, Caroline, et al. “Is radiotherapy an option for early breast cancers with complete clinical response after neoadjuvant chemotherapy?.” International Journal of Radiation Oncology* Biology* Physics 79.5 (2011): 1452-1459.

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

Haagensen, C. D., and Arthur Purdy Stout. “Carcinoma of the breast. III. Results of treatment, 1935-1942.” Annals of surgery 134.2 (1951): 151.

Herraiz, Cecilia, Eva Crosas-Molist, and Victoria Sanz-Moreno. “Reactive oxygen species and tumor dissemination: Allies no longer.” Molecular & cellular oncology 3.2 (2016): e1127313.

Hoffer, L. J., et al. “Phase I clinical trial of iv ascorbic acid in advanced malignancy.” Annals of Oncology 19.11 (2008): 1969-1974.

Ring, Alistair, et al. “Is surgery necessary after complete clinical remission following neoadjuvant chemotherapy for early breast cancer?.” Journal of clinical oncology 21.24 (2003): 4540-4545.

Seifried, Harold E., et al. “The antioxidant conundrum in cancer.” Cancer Research 63.15 (2003): 4295-4298.

Smith, Peter J., et al. “Complementary and alternative medicine use by patients receiving curative‐intent chemotherapy.” Asia‐Pacific Journal of Clinical Oncology 12.3 (2016): 265-274.

Articolul What does it mean to be cured of cancer? 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.

But the intracytoplasmic ROS level determines whether the cell progresses in the cell replication cycle or not, lower levels leading to cell cycle progression while higher ones leading to cell cycle arrest and cell death (Cairns, Harris and Mak, 2011).

Also, studies show that malignant cells have a higher tolerance for ROS than normal cells – Szatrowski and Nathan, 1991. So, to impede malignant cells survival and proliferation we need a higher level of intracytoplasmic ROS level.

And although vitamin C can act both as a pro-oxidant and antioxidant depending on the dosage, we do not know if the clinic impact of vitamin C administration is beneficial for patients with curable cancers during active oncology treatment and not during palliative care (Schumacker, 2006; Grasso et al., 2014).

Active oncology treatment with intention to cure makes the difference in what a cancer patient can or cannot take, and while there still are chances of healing antioxidants administration can decrease treatment efficacy.  

Up to now, no randomised controlled trial has proven that vitamin C has a beneficial impact in cancer patients without metastasis during chemotherapy or  radiotherapy done with intention to cure, the only benefits being increased quality of life and decreased palliative treatment toxicity in terminal cancer patients – Unlu et al., 2015; Li, Zhang and Tang, 2016

All studies showing antioxidants administration benefits are either case studies, animal studies, cell studies, studies done on incurable cancer patients or observational studies on cancer risk factors. Still the scientific interest is high, many researchers trying to prove that the improved quality of life or the decreased toxicity could be beneficial also for patients during active treatment and not only during palliation.

For instance, some researchers say cancer patients have vitamin C deficiency and therefore supplementing it would stimulate immune system and increase the quality of life of the patients, without separating either patients during active treatment from patients during palliation  or the many types of cancer.

– But what cancer patients have vitamin C deficiency?

And although many naturopaths or complementary medicine practitioners would say “all”, the study that led to this popular assumption only analysed 50 terminal cancer patients of which only 15 had low vitamin C levels. Can we just delete the other 35 and extrapolate that “cancer patients have vitamin C deficiency”? – Maryland et al., 2005

The time of diagnosis is essential when it comes to antioxidants intake impact, and there are 3 distinct periods of time:

1. before diagnosis – cancer prevention – when daily moderate intake of antioxidants naturally found in fruits, vegetables, raw seeds, legumes, lean meat, fish, whole dairy and eggs contributes up to a point to a decreased cancer risk
2. early stage diagnosis – active oncology treatement with intention to cure – when oncology nutrition is strictly personalised based on malignant metabolism, tumour localisation, treatment stage and patient comorbidities. And I would like to underline that we cannot cure cancer through nutrition, be it oral or iv, and that during active oncology treatment the main goal is treatment efficacy and not decreased treatment toxicity or increased quality of life.  During active treatment we have no proof that antioxidants have any beneficial impact on treatment efficacy.
3. late stage diagnosis or when the disease has advanced and it reached an incurable stage – palliation – when the main goals are decreased treatment toxicity or increased quality of life. And this is the only period of time when antioxidants might be useful.

Some researchers go as far as to say that the only moment when cancer patients can be administrated antioxidants without decreasing healing chances is during scientific trials – Wilson et al., 2014

Even the chemotherapy with which vitamin C is compared by complementary / integrative medicine practitioners is palliative chemotherapy not curative active treatment. – Gourgou-Bourgade et al., 2012

Chemotherapy side effects are very popular and thickly underlined by these practitioners, but most don’t also mention alternative treatments side effects because their providers are not obliged by law to prove neither their efficacy nor their safety. And of course “they are natural thus they don’t have side effects”. Cocaine is also natural.

Malignant cellular biology is extremely complex. There is a huge difference between destroying some malignant cells in a Petri dish and destroying a self-born and grown tumour in a living organism.

To understand the difference between destroying some malignant cells in a Petri dish and destroying a self-born and grown tumour in a living organism imagine trying to destroy a wasp nest.

The fact that we catch some wasps in a jar and we kill them with substance X does not mean that the whole nest will be destroyed:

• the nest might have such a complex internal structure that some wasps might not come in contact with substance X, otherwise effective if contact would occur;
• the wasps we killed in the jar with substance X might be of different age or specie than the wasps in the nest;
• and some wasps might not be in the nest when we administered the substance, thus being able to go and build another nest elsewhere.

Cancer is a heterogenous mass of cells in different stages of cell cycle able not to die. And avoiding apoptosis is very complicated, involving a whole lot of genetic modifications that make malignant cells unpredictable and very adaptable.

Assuming that vitamin C is beneficial simply because it is an antioxidant or because it might act as a pro-oxidant sounds logic and natural, and low cost, and low importance because of the supposed lack of side effects, but up to now it is just a potentially risky assumption.

– Then why it is given intravenously in high doses in some centres even alongside neoadjuvant chemotherapy, treatment also widely practiced by many naturopaths or other integrative/complementary medicine practitioners?

Maybe because 40 years ago the Nobel laureate for chemistry Linus Pauling argued that high-dose vitamin C heals or prevents cancer, the same as 400 years ago the Pope used to say that the Earth was flat. So you should had been completely out of the box to even think it is round.

– What made Pauling sustain with such vehemence vitamin C for cancer treatment?

In the ’70 Pauling and Cameron published two apparently randomised controlled studies in which they managed to highly increase the survival of terminal cancer patients to whom they administered intravenously at first and orally thereafter high doses of vitamin C – Pauling and Cameron, 1976; Pauling and Cameron, 1978

But dr. William DeWys – the head of research at US National Cancer Institute at the time – has severely criticised the validity of these studies results (Cabanillas, 2010) because:

1. the study has been restrospective and not randomised
2. and because around 20% of the patients retrospectively selected to be included in the control arm died just few days after they have been considered incurable, dr. DeWys arguing that this led to an artificially increased survival time for the vitamin C group.

Then, in 1981, Murata et al. published a study with similar retrospective design – study widely quoted at the proof that Pauling and Cameron were actually right.  – Murata, Morishige and Yamaguchi, 1981

But neither Pauling and Cameron’s studies nor Murata’s were randomised controlled trials, but restrospective ones without causal value. And what we also need to underline is that:

• all 3 studies were done on terminal cancer patients with diverse forms of cancer
• most patients died anyway within less than a year, so randomised or not, vitamin C for sure did not cure them

The hypothesis that curing cancer is as easy, simple and natural as vitamin C administration was later on contradicted by the very death of Pauling himself – who died of lung cancer in 1994 despite administering 18 g vitamin C daily.  So in his case, taking vitamin C did not prevent cancer, and did not help him cure cancer after diagnosis.

Unlike these retrospective studies, the 2 randomised controlled studies done at Mayo Clinic showed that a daily oral administration of 10g of vitamin C is of no benefit for cancer patients – Creagan et al., 1979, Moertel et al., 1985.

But the results of these studies have been disputed based on vitamin C pharmacokinetics, vitamin C supporters arguing that the antitumor effect can be obtained only through intravenous administration. – Padayatty et al., 2004

But, even for intravenous administration there are at least 3 more but:

1. despite the fact that the RDI for vitamin C is 60 mg, the supposed antitumor effect is not obtained even at doses as high as 70 g/m² administred intravenously – Hoffer et al., 2008; Stephenson et al., 2013
2. vitamin C administration can decrease oncology treatment efficacy:
   • antioxidants can decrease chemotherapy and radiotherapy efficacy – Bairati et al., 2005; Lawenda et al., 2008; Heaney et al., 2008
   • vitamin C inhibits the antitumor effect of bortezomib in patients with multiple myeloma or lymphoma – Perrone et al., 2009
3. Vitamin C does have side effects – beside gastrointestinal discomfort (diarrhea, bloating) vitamin C administration can:
   • increase iron absorption – being contraindicated in patients with hemochromatosis – Stotts and Bacon, 2017
   • increase the risk of renal oxalates lithiasis in men – being contraindicated in patients with a history of oxalic nephropathy or renal insufficiency – Massey et al., 2005; Ferraro et al., 2016
   • have a prothrombotic and procoagulant impact – being contraindicated in patients with cardiovascular disease at risk of thrombosis – Kim et al., 2015; Mohammed et al., 2017

Vitamin C is not as pink as pseudo-oncology industry would like patients to believe and the fight against cancer is far more complicated than simply taking vitamins.

In final stages, during palliative care, decreasing treatment toxicity and increasing quality of life are primary.

But during active oncology treatment for curable cancer we want the patient to feel good or we want the patient to be cured?

References

Bairati, Isabelle, et al. “Randomized trial of antioxidant vitamins to prevent acute adverse effects of radiation therapy in head and neck cancer patients.” Journal of clinical oncology 23.24 (2005): 5805-5813.

Cabanillas, Fernando. “Vitamin C and cancer: what can we conclude-1,609 patients and 33 years later.” PR Health Sci J29.3 (2010): 215-217.

Cairns, Rob A., Isaac S. Harris, and Tak W. Mak. “Regulation of cancer cell metabolism.” Nature Reviews Cancer 11.2 (2011): 85-95.

Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: prolongation of survival times in terminal human cancer. Proc Natl Acad Sci U S A 1976; 73 (10): 3685–3689.

Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: reevaluation of prolongation of survival times in terminal human cancer. Proc Natl Acad Sci U S A 1978; 75 (9): 4538–4542.

Gourgou-Bourgade, Sophie, et al. “Impact of FOLFIRINOX compared with gemcitabine on quality of life in patients with metastatic pancreatic cancer: results from the PRODIGE 4/ACCORD 11 randomized trial.” Journal of clinical oncology31.1 (2012): 23-29.

Grasso, Carole, et al. “Pharmacological doses of daily ascorbate protect tumors from radiation damage after a single dose of radiation in an intracranial mouse glioma model.” Frontiers in oncology 4 (2014).

Ferraro, Pietro Manuel, et al. “Total, dietary, and supplemental vitamin C intake and risk of incident kidney stones.” American Journal of Kidney Diseases 67.3 (2016): 400-407.

Heaney, Mark L., et al. “Vitamin C antagonizes the cytotoxic effects of antineoplastic drugs.” Cancer research 68.19 (2008): 8031-8038.

Hoffer, L. J., et al. “Phase I clinical trial of iv ascorbic acid in advanced malignancy.” Annals of Oncology (2008): mdn377.

Jacobs, Carmel, et al. “Is there a role for oral or intravenous ascorbate (vitamin C) in treating patients with cancer? A systematic review.” The oncologist 20.2 (2015): 210-223.

Kim, Keunyoung, et al. “High-Dose Vitamin C Injection to Cancer Patients May Promote Thrombosis Through Procoagulant Activation of Erythrocytes.” Toxicological Sciences 147.2 (2015): 350-359.

Lawenda, Brian D., et al. “Should supplemental antioxidant administration be avoided during chemotherapy and radiation therapy?” Journal of the national cancer institute 100.11 (2008): 773-783.

Li, F., Zhang, L., & Tang, S. C. (2016). Revisiting vitamin C in cancer therapy: Is “C” for cure, or just wishful thinking?.

Massey, Linda K., Michael Liebman, and Susan A. Kynast-Gales. “Ascorbate increases human oxaluria and kidney stone risk.” The Journal of nutrition 135.7 (2005): 1673-1677.

Mayland, Catriona R., Michael I. Bennett, and Keith Allan. “Vitamin C deficiency in cancer patients.” Palliative medicine19.1 (2005): 17-20.

Mohammed, Bassem M., et al. “Impact of high dose vitamin C on platelet function.” World journal of critical care medicine 6.1 (2017): 37.

Murata, A., F. Morishige, and H. Yamaguchi. “Prolongation of survival times of terminal cancer patients by administration of large doses of ascorbate.” International journal for vitamin and nutrition research. Supplement= Internationale Zeitschrift fur Vitamin-und Ernahrungsforschung. Supplement 23 (1981): 103-113.

Padayatty SJ, Sun H, Wang Y et al. Vitamin C pharmacokinetics: implications for oral and intravenous use. Ann Intern Med 2004; 140 (7): 533–537.

Perrone, G., et al. “Ascorbic acid inhibits antitumor activity of bortezomib in vivo.” Leukemia 23.9 (2009): 1679-1686.

Stephenson, Christopher M., et al. “Phase I clinical trial to evaluate the safety, tolerability, and pharmacokinetics of high-dose intravenous ascorbic acid in patients with advanced cancer.” Cancer chemotherapy and pharmacology 72.1 (2013): 139-146.

Stotts, Matthew J., and Bruce R. Bacon. “Metabolic and Genetic Liver Diseases: Hemochromatosis.” Liver Disorders. Springer International Publishing, 2017. 339-353.

Szatrowski, T. P., & Nathan, C. F. (1991). Production of large amounts of hydrogen peroxide by human tumor cells. Cancer research, 51(3), 794-798.

Schumacker, P. T. (2006). Reactive oxygen species in cancer cells: live by the sword, die by the sword. Cancer cell, 10(3), 175-176.

Unlu, A., Kirca, O., Ozdogan, M., & Nayır, E. (2015). Journal of Oncological Science.

Wilson, Michelle K., et al. “Review of high‐dose intravenous vitamin C as an anticancer agent.” Asia‐Pacific Journal of Clinical Oncology 10.1 (2014): 22-37.

Articolul Vitamin C for cancer patients? 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.