Why is it difficult for scientists to assess the benefits of specific products and what is still worth eating

Although you can find a lot of news about the discoveries of scientists who have proven the harm or benefits of a particular product, in reality everything is much more complicated. At least, this is the opinion of the team of scientists and doctors who jointly wrote the book “Bonus Years. An individual plan for the extension of youth based on the latest scientific discoveries. "

In it, researchers analyze the latest scientific discoveries and ways to prolong life. Including with the help of food. The fourth chapter is devoted to this topic, an excerpt from which Lifehacker publishes with the permission of the Bombora publishing house.

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There are no experiments to prove the life-prolonging properties of certain foods. Although there are many observational studies with conflicting results, this generates myths. To make at least some preliminary conclusions about the benefits of food, you need to do a lot of work, analyzing all the research carried out before this, which will reveal general trends.

It is also necessary to take into account many criteria that give grounds to establish the causal nature of the relationship of food products with benefits or harms. For the first time, such criteria were formulated by Bradford Hill, a British epidemiologist who linked smoking and lung cancer and outlined other important patterns. In a slightly modified form, Hill's criteria are usedHowick J., Glasziou P., Aronson J.K. The evolution of evidence hierarchies: what can Bradford Hill's ‘guidelines for causation’ contribute? / Journal of the Royal Society of Medicine still.

But even the beneficial or harmful effects of individual foods found in this way may be wrong. or have a minor effect, but at the same time gain notoriety similar to the notoriousness of the danger of red meat.

There is no unequivocal evidence that meat - the cause of cancer. At the same time, eating meat is very important and beneficial for the body. There is insufficient epidemiological data to conclude that mammalian meat (red) is carcinogenic. However, the huge (about 700 studies) amount of epidemiological data indicates a high probability (probability is not evidence) that meat products (sausages, bacons, etc.) are becoming cause of cancer.

Moreover, there is a possibility that this is not due to heat treatment, but, for example, the action dyes and other agents used in the industrial production of meat products, and therefore does not apply to meat in general. Epidemiological data cannot be evidence, but there is a high likelihood that meat products are the cause cancergiven the large amount of accumulated data.

Even assuming that meat products are the cause of colorectal cancer, how big is the risk? The lifetime risk of colorectal cancer for those who consume meat products is approximately 6%, and for those who do not consume it, it is 5%. Let's countWHO. Questions and answers about the carcinogenicity of red meat and meat products: 6% – 5% = 1%. In short, out of 100 people who have consumed meat products for many years, one person will get cancer for this very reason.

Is this a lot? Let's compare to smoking. The relative risk of getting cancer with the use of meat products for years is 1.18, while with long-term smoking it is equal to 30-60. Therefore, meat products are highly likely to cause colon cancer, but the risk of developing cancer is very low compared to smoking.

It is important to understand that meat products, and not any meat, are highly likely to cause cancer. Moreover, meat also has benefits. Although meat eaters dieAppleby P.N., Crowe F.L., Bradbury K.E. et al. Mortality in vegetarians and comparable nonvegetarians in the United Kingdom / The American Journal of Clinical Nutrition more often from coronary heart disease and a little more often from cancer, but less often from vascular diseases of the brain. Cardiovascular disease can be treated and risks reduced. You can even replace the heart. But dementia in particular Alzheimer's disease and vascular dementia, they still do not know how to treat, and it is pointless to transplant a new head, since it will no longer be the same person. And on average, meat eaters liveAppleby P.N., Crowe F.L., Bradbury K.E. et al. Mortality in vegetarians and comparable nonvegetarians in the United Kingdom / The American Journal of Clinical Nutrition as long as vegetarians.

Neurodegenerative diseases such as amyotrophic lateral sclerosis (damage to motor neurons brain, leading to paralysis and subsequent muscle atrophy), Alzheimer's disease (fatal senile dementia) and Parkinson's disease (tremor paralysis) pose a serious threat to human health.

Although these diseases have several specific genetic risk factors, most cases appear sporadically with no known cause. Often environmental factors combined with genetic predisposition can contribute to the onset of the disease.

One of the risk factors for the development of neurodegenerative diseases listed above may be the effect on the body of the environmental toxin β-N ‑ methylamino ‑ L ‑ alanine (BMAA). This substance can be found in high amounts in the following foods:

• spirulina (a genus of unicellular blue-green algae);
• dinophytic algae;
• diatoms;
• crustaceans;
• a fish;
• BMAA is also found in some terrestrial plants that vervet (dwarf green monkeys) eat abundantly.

Abundant consumption so popular today spirulina, crustaceans and fish can significantly increase the risk of developing neurodegenerative diseases.

Increased levels of BMAA are found in the brains of people with Alzheimer's and Parkinson's.

The diet of dwarf green monkeys contains a lot of BMAA. They have neurofibrillary tangles in their brains - accumulations of protein that are usually found in the brains of people who have died from Alzheimer's disease. In dwarf green monkeys, extracellular amyloid plaques similar to those found in which are found in people with Alzheimer's disease, Parkinson's disease, in patients with amyotrophic lateral sclerosis.

It is worth noting that BMAA interacts with neuromelanin, a form of melanin, a dark pigment. And perhaps that is why 50% of patients with Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis have rare retinopathy pigmentosa (spots in the retina) due to pigment deposits neuromelanin. BMAA studies detailPierozan P., Andersson M, Brandt I. et al. The environmental neurotoxin β-N ‑ methylamino ‑ L ‑ alanine inhibits melatonin synthesis in primary pinealocytes and a rat model / Journal of Pineal Research as a neurotoxin (toxic to the entire nervous system, and in particular to the brain).

This may be why overconsumption of fish is not good for you.Engeset D., Braaten T., Teucher B. et al. Fish consumption and mortality in the European Prospective Investigation into Cancer and Nutrition cohort / European Journal of Epidemiology. This is probably related to the observation from a prospective study that pescetarians (who do not eat meat, but eat fish) were more likely to die.Appleby P.N., Crowe F.L., Bradbury K.E. et al. Mortality in vegetarians and comparable nonvegetarians in the United Kingdom / The American Journal of Clinical Nutrition from disorders of cerebral circulation and stroke. In addition, data from the Cochrane Systematic Review indicateAbdelhamid A.S., Brown T.J., Brainard J.S. et al. Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease / Cochrane database of systematic reviewsthat the use of fish oil or the use of fish and other seafood in the analyzed randomized clinical trials did not have a significant effect on overall mortality and mortality from cardiovascular diseases.

Fried animal foods (especially fried meats) are high in glycation end products (AGEs). AGE can be a factor in aging and the development or complication of many degenerative diseases such as diabetes, atherosclerosis, chronic kidney disease and Alzheimer's disease.

The fact that AGE in fried food is harmful to diabetics has been proven in various clinical studies.

Their harm is that they, acting on the receptors of end products of glycation, increase inflammation and activate the receptors of angiotensin AT¹, increasing pressure.

A diet high in AGE is believed to have a negative effect on health, increase blood pressure and increase the content of markers of inflammation. A randomized, double-blind, crossover study was conducted to determine if diet reduced low AGE, inflammation and cardiovascular risks with overweight and obesity, but no sugar diabetes. All participants consumed low and high CNG foods alternately for two weeks.

A diet low in AGE did not alter systolic and diastolic blood pressure, mean arterial pressure, and pulse pressure when compared to a diet high in AGE. General levels cholesterol, low density lipoproteins, high density lipoproteins and triglycerides also did not differ, did not there was a statistically significant difference in the levels of inflammatory markers: interleukin-6 and C-reactive protein.

These findings suggest that two-week low-AGE diets did not improveBaye E., de Courten M.P., Walker K. et al. Effect of dietary advanced glycation end products on inflammation and cardiovascular risks in healthy overweight adults: a randomized crossover trial / Scientific Reports inflammatory and cardiovascular profiles in overweight and obese adults without sugar diabetes.

Another study investigated not only the effect of AGE, but also the importance of the presence or absence of plant fiber in increasing the glycemic load of food consumed by people without diabetes. In essence, a comparison was made between a diet high in ANG that was low in fiber versus a diet that was low in ANG and high in fiber.

The less plant fiber in food, the higher its glycemic load.

If AGE is negatively affected, markers of inflammation and blood pressure should rise. If the high glycemic load is negatively affected, then in addition, insulin sensitivity should decrease.

However, inflammatory markers did not change, but only insulin sensitivity changed, which shows that, possibly, the presence of AGE in food on healthy people for four weeks did not have a negative effect, only a high glycemic load had a negative effect, reducing the sensitivity to insulin.

In this study, eating a high glycemic load increased the concentration of plasminogen activator inhibitor-1 (PAI-1). An increased concentration of PAI-1 can be a very early marker of the risk of insulin resistance leading to type 2 diabetes mellitus.

What conclusions can be drawn? The studies lasted four and two weeks. Will it make any difference if healthy people consume food with a high CNG content only for a year? We don't know yet.

Probably, sometimes eating fried chicken in shawarma with a lot of fresh vegetables is quite harmless for a healthy person, especially for an athlete who is much more protected.Kim Y., Keogh J.B., Clifton P.M. Effects of Two Different Dietary Patterns on Inflammatory Markers, Advanced Glycation End Products and Lipids in Subjects without Type 2 Diabetes: A Randomized Crossover Study / Nutrients from foods with a high glycemic load.

Negative attitude towards coffee has a long history. In 1511, coffee was banned in Mecca: it was believed that drinking coffee provokes rebellious moods. In 1677, the English king Charles II banned coffee houses. The pretext was a written complaint from the ladies that their husbands, addicted to coffee, had ceased to fulfill their marital duties. In 1746, the Swedish government banned not only coffee, but even coffee utensils, including cups and saucers. In 1777, the Prussian king Frederick the Great issued a manifesto urging his subjects to give up coffee and drink beer.

Coffee is one of the most popular drinks with a controversial reputation. Everyone knows that excessive consumption of coffee raises blood pressure and causes heartbeat. Therefore, many people intuitively consider coffee harmful to the heart and blood vessels.

In studies, caffeine prolonged 1. Lublin A., Isoda F., Patel H. et al. FDA-approved drugs that protect mammalian neurons from glucose toxicity slow aging dependent on cbp and protect against proteotoxicity / PLoS One;
2. Bridi J.C., Barros A.G., Sampaio L.R. et al. Lifespan Extension Induced by Caffeine in Caenorhabditis elegans is Partially Dependent on Adenosine Signaling / Frontiers in Aging Neuroscience life of animals. Excessive consumption of coffee is unhealthy, but numerous studies involving many hundreds of thousands of people united by meta-analyzes of meta-analyzes, moderate coffee consumption (1-3 cups per day) connectedPoole R., Kennedy O.J., Roderick P. et al. Coffee consumption and health: umbrella review of meta-analyzes of multiple health outcomes / BMJ with many positive effects: a reduction in the risk of overall mortality and a 20% reduction in the risk of mortality from cardiovascular diseases; with lowerChoi H.K., Curhan G. Coffee, tea, and caffeine consumption and serum uric acid level: the third national health and nutrition examination survey / Arthritis & Rheumatology serum uric acid levels, which are beneficial for the prevention of urolithiasis and goutZhang Y., Yang T., Zeng C. et al. Is coffee consumption associated with a lower risk of hyperuricaemia or gout? A systematic review and meta ‑ analysis / BMJ Open; reducing the risk of developing Parkinson's diseaseHerraiz T., Chaparro C. Human monoamine oxidase enzyme inhibition by coffee and beta-carbolines norharman and harman isolated from coffee / Life Sciences and Alzheimer'sVan Gelder B.M., Buijsse B., Tijhuis M. et al. Coffee consumption is inversely associated with cognitive decline in elderly European men: the FINE Study / European Journal of Clinical Microbiology & Infectious Diseases (probably protects brain cells from aging); reducing the risk of diabetesDing M., Bhupathiraju S.N., Chen M. et al. Caffeinated and decaffeinated coffee consumption and risk of type 2 diabetes: a systematic review and a dose ‑ response meta ‑ analysis / Diabetes Care Type 2, cardiovascular disease, the development of depressionWang L., Shen X., Y. et al. Coffee and caffeine consumption and depression: A meta-analysis of observational studies / Australian and New Zealand Journal of Psychiatry and suicideLucas M., O'Reilly E. J., Pan A. et al. Coffee, caffeine, and risk of completed suicide: results from three prospective cohorts of American adults / The World Journal of Biological Psychiatry, cirrhosisKennedy O.J., Roderick P., Buchanan R. et al. Systematic review with meta-analysis: coffee consumption and the risk of cirrhosis / Alimentary Pharmacology & Therapeutics and aging, gallstone formation; with less risk of liver cancer 1. Malerba S., Turati F., Galeone C. et al. A meta ‑ analysis of prospective studies of coffee consumption and mortality for all causes, cancers and cardiovascular diseases / European Journal of Epidemiology;
2. Cardin R., Piciocchi M., Martines D. et al. Effects of coffee consumption in chronic hepatitis C: a randomized controlled trial / Digestive and Liver Disease, kidneys 1. Malerba S., Turati F., Galeone C. et al. A meta ‑ analysis of prospective studies of coffee consumption and mortality for all causes, cancers and cardiovascular diseases / European Journal of Epidemiology;
2. Wijarnpreecha K., Thongprayoon C., Thamcharoen N. et al. Association between coffee consumption and risk of renal cell carcinoma: a meta ‑ analysis / Journal of Internal Medicine, premenopausal breast cancer 1. Malerba S., Turati F., Galeone C. et al. A meta ‑ analysis of prospective studies of coffee consumption and mortality for all causes, cancers and cardiovascular diseases / European Journal of Epidemiology;
2. Lafranconi A., Micek A., De Paoli P. et al. Coffee Intake Decreases Risk of Postmenopausal Breast Cancer. A Dose-Response Meta-Analysis on Prospective Cohort Studies / Nutrients and colon cancerMalerba S., Turati F., Galeone C. et al. A meta ‑ analysis of prospective studies of coffee consumption and mortality for all causes, cancers and cardiovascular diseases / European Journal of Epidemiology.

But drinking coffee is related 1. Guessous I., Dobrinas M., Kutalik Z. et al. Caffeine intake and CYP1A2 variants associated with high caffeine intake protect non-smokers from hypertension / Human Molecular Genetics;
2. Cornelis M.C., El-Sohemy A., Kabagambe E.K., Campos H. Coffee, CYP1A2 genotype, and risk of myocardial infarction / JAMA;
3. Palatini P., Benetti E., Mos L. et al. Association of coffee consumption and CYP1A2 polymorphism with risk of impaired fasting glucose in hypertensive patients / European Journal of Epidemiology with a higher risk of heart attack only in those whose cytochrome P450 1A2 does not work well, which is involved in the metabolism of xenobiotics in the body, moreover, if you drink more than three cups a day. In general, for humans, drinking more than 2-3 cups of coffee per day is associated with a higher risk of death from cardiovascular disease.

Consuming unfiltered coffee leads to an increase in bad cholesterol - low-density lipoprotein and triglyceride levels, as well as an increase sugar level fasting and inflammatory markers.

But filtered coffee does not affect cholesterol levels and reducesRebello S.A., van Dam R.M. Coffee consumption and cardiovascular health: getting to the heart of the matter / Current Cardiology Reports inflammatory markers. Need to drinkLopez-Garcia E., van Dam R.M., Qi L., Hu F.B. Coffee consumption and markers of inflammation and endothelial dysfunction in healthy and diabetic women / The American Journal of Clinical Nutrition only filtered coffee or instant coffee.

It is undesirable to drink coffee for those who use 1. Chen Y., Liu W.H., Chen B.L. et al. Plant polyphenol curcumin significantly affects CYP1A2 and CYP2A6 activity in healthy, male Chinese volunteers / Annals of Pharmacotherapy;
2. Fontana R.J., Lown K.S., Paine M.F. et al. Effects of a chargrilled meat diet on expression of CYP3A, CYP1A, and P ‑ glycoprotein levels in healthy volunteers / Gastroenterology oral contraceptives, fluvoxamine, turmeric, cumin, mint, chamomile, dandelions, St. John's wort. Cannot be consumedLi M., Wang M., Guo W. et al. The effect of caffeine on intraocular pressure: a systematic review and meta ‑ analysis / Graefe's Archive for Clinical and Experimental Ophthalmology coffee for severe liver diseases, hypertension, glaucoma.

What should our diet consist of?

While general principles of nutrition, such as lowering glycemic load, moderation in food, are well researched, then there is very little evidence for individual foods. The gold standard of evidence for life extension is a long-term randomized clinical trial with a mortality endpoint.

Such food tests have not been conducted. However, a huge number of observational studies have been carried out, based on which it is possible to buildHowick J., Glasziou P., Aronson J.K. The evolution of evidence hierarchies: what can Bradford Hill's ‘guidelines for causation’ contribute? / Journal of the Royal Society of Medicine hypotheses using the Bradford Hill test. The most probable of them are named by WHO.

So what is most likely to be beneficial?

The American Cancer Institute recommends including whole grains as the basis of the daily diet. (e.g. brown rice, wheat, oats, barley and rye), non-starchy vegetables and fruits, nuts, beans, lentils.

Or rather, consume at least 30 g of fiberLustgarten M. High ‑ Fiber Diets Are Associated With Reduced All ‑ Cause Mortality Risk and at least 400 g of fruits and non-starchy vegetablesAmerican Institute for Cancer Research. Eat wholegrains, vegetables, fruit & beans in a day. Of vegetables, tomatoes are the most beneficial for health and are associated with a decrease in the risk of mortality. 1. Cheng H.M., Koutsidis G., Lodge J.K. et al. Tomato and lycopene supplementation and cardiovascular risk factors. A systematic review and meta ‑ analysis / Atherosclerosis;
2. Cheng H.M., Koutsidis G., Lodge J.K. et al. Lycopene and tomato and risk of cardiovascular diseases: A systematic review and meta ‑ analysis of epidemiological evidence and all varieties of cabbage 1. Zhang X., Shu X.O., Xiang Y.B. et al. Cruciferous vegetable consumption is associated with a reduced risk of total and cardiovascular disease mortality / The American Journal of Clinical Nutrition;
2. Aune D., Giovannucci E., Boffetta P. et al. Fruit and vegetable intake and the risk of cardiovascular disease, total cancer and all-cause mortality-a systematic review and dose-response meta-analysis of prospective studies / International Journal of Epidemiology;
3. Mori N., Shimazu T., Charvat H. et al. Cruciferous vegetable intake and mortality in middle-aged adults: A prospective cohort study / Clinical Nutrition.

As a matter of fact, that's all for now. The data for other food groups are not convincing enough - they are either few or contradictory. In 2013 statisticians John Ioannidis and Jonathan Schonfeld reviewed the Boston Cooking School Cookbook and randomly selectedSchoenfeld J.D., Ioannidis J.P.A. Is everything we eat associated with cancer? A systematic cookbook review / The American Journal of Clinical Nutrition from it several recipes, which in total contained 50 ingredients.

They then searched PubMed's scientific research database to find studies examining the relationship of each ingredient to cancer risk. Studies have yielded mutually exclusive results: eating the same food for the results of some studies were associated with an increased risk of cancer, according to the results of others - vice versa. Where do such contradictions come from?

Cancer is not one but hundreds of different diseases with different causes. Therefore, it makes sense that the same substance can increase the risk of one type of cancer and reduce the likelihood of developing another type of tumor.

In different periods of life (old age and youth), different food products affect us in different ways.

Communication is not a reason. For example, coffee may be linked to lung cancer in observational studies because coffee drinkers are more likely to smoke. And it's not coffee that causes cancer, it's smoking. But an observational study cannot find the reason coffee is linked to cancer, it can only reveal the link. There are few studies on the effects of food on mortality risk.

This is not surprising: conducting randomized trials is much more difficult and expensive. At the same time, it is especially difficult to study with their help the effect of nutrition on the body: you should not expect that all volunteers, randomly assigned to one group or another, will obediently eat for many years exactly as they were prescribed in research.

Eating expensive foods can also increase lifespan. But this may not be due to the properties of the products, but to the fact that people with a higher income who consume them, in principle, liveAttanasio O.P., Emmerson C. Mortality, Health Status, and Wealth / Journal of the European Economic Association longer, possibly due to the availability of a higher standard of medicine.

It is useless to draw conclusions from individual publications of such observational studies. Fashionable diets and healthy foods are described in beautiful books on store shelves. Online stores are overflowing with medicinal dietary supplements based on supposedly beneficial ingredients, tested mainly on animals and in separate observational studies.

So, to increase the likelihood of living longer, you need to reduce the glycemic load of your diet. In this case, the basis of the diet should be non-starchy vegetables and fruits, as well as legumes, whole grains, nuts, olive oil. The rest of the products are optional.

After age 65, it is especially important that the diet contains a sufficient amount of animal protein (meat, cheese, cottage cheese, poultry). Patients with diabetes mellitus are advised to avoid eating fried animal products. However, the inclusion of fried meat in the diet of healthy people is sometimes acceptable.

If you are looking to learn how to live longer, Bonus Years is the right guide. The authors provide practical advice based on the latest scientific research.

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