Eating a moderate amount of carbohydrates best for healthy lifespan, say researchers
Eating either a low-carb diet or a high-carb diet creates the risk of an early death, according to a major new study which will dismay the many people who have ditched the likes of bread, rice and potatoes for weight loss or health reasons.
Researchers who pooled the results of eight big studies have found that eating a moderate sum of carbohydrates is best for a healthy lifespan. Less than 40% or more than 70% of calories from carbohydrates carried a higher risk of mortality.
Not all low-carb diets are equal, however. People who ate a lot of meat and fats instead of carbohydrates, such as lamb, chicken, steak, butter and cheese, had a higher mortality risk than those who got their protein and fats from plant-based foods such as avocados, legumes and nuts. Popular weight loss diets such as Atkins and Dukan include a substantial amount of meat-based foods.
” Low-carb diets that replace carbohydrates with protein or fat are gaining widespread popularity as a health and weight loss strategy ,” said Dr Sara Seidelmann, a clinical and research fellow in cardiovascular medication from Brigham and Women’s Hospital inBoston, who led the research published in the Lancetpublichealth journal.
” However, our data suggests that animal-based low-carbohydrate diets, which are prevalent in North America and Europe, might be associated with shorter overall life span and should be discouraged. Instead, if one chooses to follow a low-carbohydrate diet, then exchanging carbohydrates for more plant-based fats and proteins might actually promote healthy ageing in the long term .”
Seidelmann, who is both a cardiologist and a nutritionist, told the Guardian the team had published a substantial body of work” to exhaustively answer a question and not simply offer merely one piece of the picture “.
” Nutrition is high up on everybody’s intellect but there is such embarrassment about what we should eat. One day, a study is coming out telling us high carb is better, another day a study is telling us low carb is better .”
Trials to compare low-carb and high-carb diets immediately are not possible, because they have to be carried out over many years and people find it hard to stick to a diet over any duration of period. Instead, her squad carried out observational research with more than 15,400 people, aged 45 to 64, from diverse socio-economic backgrounds from four US communities who were enrolled in the atherosclerosis risk in communities study. Those people filled out questionnaires on their eating patterns on two occasions, six years apart. Their health was followed up for 25 years, allowing for factors that might alter the results, such as smoking, income and diabetes.
These results were pooled with seven other observational studies carried out in various regions of the world, involving a total of more than 430,000 people.
They found that 50 -year-olds eating a moderate carb diet, with half their energy coming from carbohydrates, had a further life expectancy of 33 years, which was four years longer than those on low-carb diets and one year longer than those who feed a high-carb diet.
The writers said they could not prove cause and effect, because of the nature of the studies. However, they said people who embraced western-type diets that heavily restricted carbohydrates often ate fewer veggies, fruit, and grains and more animal proteins and fats. Some of those animal products have been implicated in stimulating inflammatory pathways, biological ageing and oxidative stress, and could be a contributing factor to the increased risk of mortality.
High-carb diets are common in Asian and poorer nations, they said, where people eat a lot of refined carbohydrates such as white rice. Those also contribute to a chronically high glycaemic load and worse metabolic outcomes.
” These findings bring together several strands that ought to have controversial. Too much and too little carbohydrate can be harmful but what counts most is the type of fat, protein, and carbohydrate ,” said Walter Willett, a prof of epidemiology and nutrition at Harvard T H Chan School of Public Health and the co-author of the study.
Low-carb diets are popular for weight loss because they work quite well in the short term, said Seidelmann, and they are usually meat-based. The study was not set up in a way that would make it possible to compare moderate carb with low-carb plant-based diets but, said Seidelmann,” the more plant-based[ the diet was ], the lower the mortality “.
” No facet of nutrition is so heatedly argued on social media than the carb versus fat debate, despite the long term evidence on health benefits firmly supporting the higher carb argument ,” said Catherine Collins, an NHS dietitian.
The” cult of low carb high fat eating” was based on a lifestyle choice and the flimsiest of evidence, she said. Its devotees were” at odds with advice from WHO and government health bodies globally- including the UK’s Public Health England- that recommend a carb intake to provide around half our daily calorie needs “.
She added that it the findings raise questions about the current hyping of low-carb diets for people with diabetes.” The feting and promotion of GPs promoting often bizarre low carb diets to manage diabetes has gained much media traction ,” she said.” If nothing else, this study offer some redress to this one-sided debate, and adds caution to such practice for long term management .”
In a commentary in the publication, Dr Andrew Mente and Dr Salim Yusuf, from McMaster University in Canada, said it was not possible to rule out altogether all the factors that might skewed the results, but that the findings were that logical and moderate carbohydrate intake was likely to be better for people than low or high-carb diets.
” Essential nutrients should be consumed above a minimal level to avoid deficiency and below a maximal level to avoid toxicity. This approach maintains physiological processes and health( ie, a so-called sweet spot ). Although carbohydrates are technically not an essential nutrient( unlike protein and fats ), a certain amount is probably required to meet short-term energy demands during physical activity and to maintain fat and protein uptakes within their respective sweet places ,” they wrote.
Do whole grains avoid diabetes? Is moderate drinking good or bad for you? Nutritional studies are more complex than you are told
There’s a news cycle that we have all become attuned to. It’s what has led various publications to conclude that broccoli is both cause and avoiding cancer, that chocolate is a weight-loss food and a diet murderer, and that diet soft drink, against all odds, are causing people to gain weight.
This is the world of nutritional epidemiology. And it is complex.
Most recently we’ve been told that whole grains- the minimally-processed foods such as rye bread that contain high levels of fibre- are the key to preventing diabetes.
And while there is no argument that whole grains are good for you, or at the very least far better than the highly-processed alternatives, the claim that they avoid diabetes is much harder to justify.
Nutritional epidemiology is fascinating, but many people who comment on it do not discuss the above intricacies of the situation. Which is a problem, when an entire field is built on nuance.
Grains are good
The most recent study was a piece of epidemiological magnificence. The researchers took a large sample of people who had given information on how many grains they eat, and seemed to see if grain intake was correlated with diabetes. They also controlled for a number of factors, including age, gender, and socio-economic status, making their results actually quite good.
The study found that people who ate more whole grains, including with regard to rye bread, were less likely to get diabetes. There was even what’s known as a biological gradient- the more grains the study participants ate, the less likely they were to get diabetes.
If this sounds very convincing, that’s because it really was an excellent study.
But there are some important restrictions that most people did not discuss and that mean that it may have very little relevance to your life at all.
The biggest issue with all nutritional epidemiology studies is something known as residual confounding. Confounding is the process that occurs when issues external to a study are not taken into account. So, for example, if you are studying the rate of deaths caused by falling out of an airplane, but don’t know how many of your participants were wearing parachutes, you might conclude that actually it’s pretty safe. The problem with epidemiological trials like this is that you can account for many factors but you just can’t account for everything.
The recent study on grains accounted for a lot of things, but ultimately there are likely still residual the matters that they just can’t address. The people in this study who eat more grains were thinner, better-educated, more active, less likely to smoke, and other good things, than the ones who ate the least grains. It is highly likely that there exist residual factors that the researchers could not takes into consideration that may have caused the people who eat the most grains to be healthier — and thus, less likely to have diabetes — than the people who feed less grains.
There were other points in the study that make interpreting somewhat problematic. For one thing, the absolute danger discrepancies between the highest and lowest grain uptake groups was just 4 %, which is much less than the relative difference reported on in the majority media narratives. This was also a study in Danish people over the age of 50, which means that it’s very difficult to generalise the findings to people living elsewhere.
And sadly, this sort of intricacy is common. Misunderstanding happens all the time.
Remember the recent stories about cheese protecting against all-cause mortality? Or the news that high-carb diets were bad followed six months later with the contradiction that they were actually good? Or hearing that moderate drinking is both good and bad for your health?
All of these conclusions were derived from similar studies.
Most of them are wrong.
The problem here is that nutritional epidemiology is a really complex field. Construing results isn’t something you can easily do, especially based on one study. Whether cheese protects against all-cause mortality — the evidence very unclear — is a difficult question, fraught with confounders. The same is true for grains: it is extremely likely that someone who replaces the white bread in their diet with rye will be enhanced their health, but if you already eat mostly fresh fruit and veggies it’s unclear whether adding whole grains will help. You might just be healthier because you are rich enough to afford whole grains rather than regular wheat, and this comes with a host of health benefits.
And this is in one of the strongest the sectors of nutritional epidemiology: leaving this particular study aside, there is strong and consistent evidence that eating whole grains in your diet is associated with a range of good health outcomes.
Ultimately, the point is that these large studies, while interesting to epidemiologists like me, are not really that important for any individual person’s life. Whole grains are a part of many healthy diets, but it’s hard to generalise that to everyone.
The best diet is the one that works for you. If you need help with that, big epidemiological trials will, at best, confound you. Talk to a registered dietitian. They go through lengthy degrees and training to give you the best advice possible on your diet.
Just don’t listen to the headlines. Even if they’re right, they are probably wrong for you.
* Gideon Meyerowitz-Katz is an epidemiologist working in the field of chronic disease
The long read: The oh-so-Instagrammable food movement has been thoroughly debunked but it shows no signs of going away. The real question is why we were so desperate to believe it
In the spring of 2014, Jordan Younger “ve noticed that” her hair was falling out in clumps.” Not cool” was her reaction. At the time, Younger, 23, believed herself to be eating the healthiest of all possible diets. She was a” gluten-free, sugar-free, oil-free, grain-free, legume-free, plant-based raw vegan “. As The Blonde Vegan, Younger was a “wellness” blogger in New York City, one of thousands on Instagram( where she had 70,000 followers) rallying under the hashtag #eatclean. Although she had no qualifications as a nutritionist, Younger had sold more than 40,000 copies of her own $25, five-day “cleanse” programme– a formula for an all-raw, plant-based diet majoring on green juice.
But the “clean” diet that Younger was selling as the route to health was making its inventor sick. Far from being super-healthy, she was suffering from a serious eating disorder: orthorexia, an preoccupation with ingesting merely foods the hell is pure and perfect. Younger’s raw vegan diet had caused her periods to stop and devoted her skin an orange tinge from all the sweet potato and carrots she ingested( the only carbohydrates she permitted herself ). Eventually, she tried psychological assistance, and began to slowly widen the repertoire of foods she would allow herself to feed, beginning with the fish. She recognised that their own problems was not her veganism, per se, but the particularly rigid and restrictive diet regime she had imposed under herself.
As Younger slowly recovered from her eating disorder, she faced a new dilemma.” What would people believe”, she agonised,” if they knew the Blonde Vegan was feeing fish ?” She levelled with her adherents in a blogpost entitled Why I’m Transitioning Away from Veganism. Within hours of announcing her new diet, Younger was receiving irate messages from vegans demanding fund back from the cleanse programmes and T-shirts they had bought from her site( featuring slogans such as” OH KALE YES “).
She lost followers “by the thousands” and received a daily raft of angry messages, including death threats. Some responded to her confession that she was suffering from an eating disorder by accusing her of being a” fat piece of lard” who didn’t have the discipline to be truly “clean”.
For as long as people have feed food, there have been diets and quack remedies. But previously, these existed, like conspiracy hypothesis, on the fringes of food culture.” Clean feeing” was different, because it established based as significant challenges to mainstream ways of eating, and its wild popularity over the past five years has enabled it to move far beyond the fringes. Powered by social media, it has been more absolutist in its claims and more popular in its reaching than any previous school of modern nutrition advice.
At its simplest, clean feeing is about ingesting nothing but “whole” or “unprocessed” foods( whatever is meant by these deep equivocal terms ). Some versions of clean eating have been vegan, while others espouse various meats( preferably wild) and something mysteriously called ” bone broth“( stock, to you and me ). At first, clean eating sounded modest and even homespuns: rather than counting calories, you would eat as many nutritious home-cooked substances as possible.
But it quickly became clear that” clean eating” was more than a diet; it was a belief system, which propagated the idea that the way most people feed is not simply fattening, but impure. Seemingly out of nowhere, a whole cosmo of coconut oil, dubious promises and spiralised courgettes has emerged. Back in the remote mists of 2009, James Duigan, owned of The Bodyism gym in London and sometime personal trainer to the model Elle MacPherson, published his first Clean and Lean book. As an early adopter of #eatclean, Duigan notes that he “battled” with his publisher” to include ingredients like kale and quinoa, because no one had ever heard of them “. Now quinoa is in every supermarket and kale has become as normal as lettuce.” I long for the working day when clean eating entailed not getting too much down your front ,” the novelist Susie Boyt joked recently.
Randy is 62 years old and stands tall at six foot one. He grew up on a farm in Glasford, Illinois, in the 1950s. Randy was raised with the strong discipline of a farming family. From the time he was five, he would get out of bed at dawn, and before breakfast hed put on his boots and jeans to milk cows, lift hay, and clean the chicken coops. Day in and out, no matter the weather or how he felt, Randy did his physically demanding chores. Only when his work was complete would he come into the kitchen for breakfast.
Tending to the chickens was hard workit involved getting into the pen, clearing birds out of their dirty cages, and shooing them into a holding enclosure. This process was always a little scary because the animals could be quite aggressive after being cooped up all night. On one of these occasions, when Randy was 11, a particularly large and perturbed rooster swung its claw and gave him a good spurring on his leg. Randy felt the piercing of his skin and squealed in pain. He said it felt like being gored by a thick fishhook. The rooster left a long gash, and blood streamed down Randys leg to his ankle. He ran back to the house to clean the wound, as chickens are filthy after a night in their cages.
Some days later, Randy noticed a change in his appetite. He was constantly hungry. He felt drawn to food and thought about it all the time. He started eating in between meals and overeating when he finally sat down to dinner. Randy had always been a skinny kid, but in the course of the next year, he gained about 10 pounds. His parents thought it might be puberty, though it seemed a little early. His pudginess was also unusual given that everyone else in the family was thin. Randy was no stranger to discipline. He forced himself to eat less, switched to lower-calorie foods and exercised more. But by the time he was a teenager, he was bouncing between 30 and 40 pounds overweight. He says, I gained all of this weight even though these were some of my most active years on the farm.
Randys family supported his efforts to control his weight. They made lower-calorie foods, gave him time to exercise, and didnt pressure him to eat things he didnt want. However, he continued to struggle with his weight through college. Randy kept thinking back to the moment everything changed. He had been the skinniest kid among his friends. And then he got cut by that chicken.
The Curious Case of Indian Chickens
In Mumbai, India, Nikhil Dhurandhar followed his father Vinods footsteps in treating obesity. But Nikhil ran into the same obstacle that had bedeviled obesity doctors everywhere. The problem was that I was not able to produce something for patients that could have meaningful weight loss that was sustainable for a long time, he says. Patients kept coming back.
Fate intervened in Dhurandhars life one day was when he was meeting his father and a family friend, S. M. Ajinkya, a veterinary pathologist, for tea. Ajinkya described an epidemic then blazing through the Indian poultry industry killing thousands of chickens. He had identified the virus and named it using, in part, his own initialsSMAM-1. Upon necropsy, Ajinkya explained, the chickens were found to have shrunken thymuses, enlarged kidneys and livers, and fat deposited in the abdomen. Dhurandhar thought this was unusual because typically viruses cause weight loss, not gain. Ajinkya was about to go on, but Dhurandhar stopped him: You just said something that doesnt sound right to me. You said that the chickens had a lot of fat in their abdomen. Is it possible that the virus was making them fat?
Ajinkya answered honestly, I dont know, and urged Dhurandhar to study the question. That fateful conversation set Dhurandhar on a path to investigate as part of his PhD project whether a virus could cause fat.
Dhurandhar pushed ahead and arranged an experiment using 20 healthy chickens. He infected half of them with SMAM-1 and left the other half uninfected. During the experiment, both groups of chickens consumed the same amount of food. By the end of the experiment, only the chickens infected with the SMAM-1 virus had become fat. However, even though the infected chickens were fatter, they had lower cholesterol and triglyceride levels in their blood than the uninfected birds. It was quite paradoxical, Dhurandhar remembers, because if you have a fatter chicken, you would expect them to have greater cholesterol and circulating triglycerides, but instead those levels went in the wrong direction.
To confirm the results, he set up a repeat experiment, this time using 100 chickens. Again, only the chickens with the SMAM-1 virus in their blood became fat. Dhurandhar was intrigued. A virus, it seemed, was causing obesity. Dhurandhar thought of a way to test this. He arranged three groups of chickens in separate cages: one group that was not infected, a second group that was infected with the virus, and a third group that caged infected and uninfected chickens together. Within three weeks, the uninfected chickens that shared a cage with infected ones had caught the virus and gained a significant amount of body fat compared to the isolated uninfected birds.
Fat, it seemed, could indeed be contagious.
Now, Dhurandhar is a man of science. He is rational and calm. But even he had to admit that the idea was startling. Does this mean that sneezing on somebody can transmit obesity? This now seemed possible in animals, but what about humans? Injecting the virus into people would be unethical, but Dhurandhar did have a way to test patients to see if they had contracted the virus in the past.
Dhurandhar says, At that time I had my obesity clinic, and I was doing blood tests for patients for their treatment. I thought I might just as well take a little bit of blood and test for antibodies to SMAM-1. Antibodies would indicate whether the patient was infected in the past with SMAM-1. The conventional wisdom is that an adenovirus for chickens does not infect humans, but I decided to check anyway. It turned out that 20 percent of the people we tested were positive for antibodies for SMAM-1. And those 20 percent were heavier, had greater body mass index and lower cholesterol and lower triglycerides compared to the antibody-negative individuals, just as the chickens had. Dhurandhar observed that people who had been infected with SMAM-1 were on average 33 pounds heavier than those who werent infected.
The Pounds Keep Coming
While Nikhil Dhurandhar was in India pursuing his curiosity about fat, Randy was looking for solutions of his own. After a brief stint as a teacher he moved back to the family land in 1977 because he loved farming.
Randy married and had four children. At family dinners and holiday gatherings, he ate alongside everyone else, but tried eating less than the others. Still, his weight ballooned; by his late 30s he had topped 300 pounds. He remembers feeling hungry all the time, though even when he abstained it didnt help him lose weight. I could have several good weeks of eating stringently, much less than others around me, but if I went off my diet for just one mealboom, the weight would come back.
The effort to control his eating, even when it was successful, made Randy miserable: I cant tell you what it is like to be hungry all the time. It is an ongoing stress. Try it. Most people who give advice dont have to feel it.
In the fall of 1989, Randy applied for a commercial drivers license. The application required a medical exam. After his urine test, the nurse asked Randy if he felt all right. Normal for the day, he replied. But the nurse told Randy he would have to give a blood sample because she thought the lab had spilled glucose solution into his urine sample. The blood work showed that Randys glucose level was near 500 mg/dL (a normal reading is 100). The lab hadnt made a mistake with the urine sample after all; Randys numbers were just off the charts. Alarmed, the nurse notified Randys doctor, who then tested him for fasting blood sugar levels. The results showed that Randy had insulin resistance and severe diabetes.
At 40 years old and 350 pounds, Randy was in trouble. If he didnt fix this problem soon, he would start to develop serious complications of diabetes, including cardiovascular disease and nerve damage.
Having tried and failed multiple diets, Randy and his doctor decided the best hope was a hospital program for severe diabetics. The staff tested Randys blood frequently to determine the optimal dosage and timing of insulin injections to regulate his blood sugar. Randy learned about the Diabetic Exchange diet, which allots patients a specific number of servings of meat, carbohydrates, vegetables, and fat. He cut out all refined carbohydrates, including bread. He says, I havent had a slice of bread or piece of pizza in years.
But would even this program be enough? Randy had always had a difficult time controlling his weight, though not for lack of trying. He had been fighting fat since his childhood by controlling portions, exercising, and avoiding social eating. But his discipline was no match for his own fat. Randy had to get his weight under control permanently. The hospital environment was helpful. However, despite strictly adhering to the diet, he only dropped a few pounds.
The Virus in Americans
After taking on a postdoctoral fellowship at the University of Wisconsin, Madison under Dr. Richard Atkinson, Dhurandhar was excited to finally be at liberty to pursue what he loved. He had an intense curiosity about viruses and was eager to get started finding answers. However, when he tried to get samples of the SMAM-1 virus that he had worked with in India, the U.S. Department of Agriculture refused to grant him an import license. He was deeply disappointed.
Unable to get SMAM-1, Dhurandhar approached a company that sells viruses for research. Their catalog listed some fifty human adenoviruses. He says, I was going to order the human adenovirus, but there was no the adenovirusthere were 50 different human adenoviruses! So I was stuck again. I wondered how do I go about this? Should we start number one, number two, number three, number 50, 49, 48? So [with] a little bit of guesswork and mostly luck, we decided to work with number 36. We liked number 36 because it was antigenically uniquemeaning it did not cross react with other viruses in the group, and antibodies to other viruses would not neutralize it.
That was a serendipitous choice. It turned out that Ad-36 had similar qualities to SMAM-1 in chickens. Atkinson thought Ad-36 might very well be a mutated form of SMAM-1. When Dhurandhar infected chickens with Ad-36, their fat increased and their cholesterol and triglycerides decreased, just as had happened with SMAM-1. Dhurandhar wanted to make sure he was not getting a false positive, so he injected another group of chickens with a virus called CELO to ensure that other viruses were not also producing fat in chickens. Additionally, he maintained a group of chickens who had not been injected with anything. When he compared the three groups, only the Ad-36 group became fatter. Dhurandhar then tried the experiments in mice and marmosets. In every case, Ad-36 made animals fatter. Marmosets gained about three times as much weight as the uninfected animals, their body fat increasing by almost 60 percent!
Now came the big question: would Ad-36 have any effect on humans? Dhurandhar and Atkinson tested over 500 human subjects to see if they had antibodies to the Ad-36 virus, indicating they had been infected with it at some point in their lives. His team found that 30 percent of subjects who were obese tested positive for Ad-36, but only 11 percent of nonobese individuals dida 3 to 1 ratio. In addition, nonobese individuals who tested positive for Ad-36 were significantly heavier than those who had never been exposed to the virus. Once again, the virus was correlated with fat.
Next, Dhurandhar devised an even more stringent experiment. He tested pairs of twins for presence of Ad-36. He explains, It turned out exactly the way we hypothesizedthe Ad-36 positive co-twins were significantly fatter compared to their Ad-36 negative counterparts.
Of course, its unethical to infect human subjects with viruses for research, so the study cant be perfectly confirmed. But, Dhurandhar says, This is the closest you can come to showing the role of the virus in humans, short of infecting them.
A New Way to Manage FatStop the Blame
Randys physician had been treating him for years and knew that his patients struggle was difficult and ongoing. The physician referred Randy to an endocrinologistRichard Atkinson at the University of Wisconsinwho was having some success with difficult obesity cases.
Randy went to see Atkinson, knowing that if he didnt get his fat under control, it was going to kill him. The first thing Randy noticed about Atkinson was that he was kind. He didnt make Randy feel guilty about his weight. Other places put the blame on you, Randy says. They go back into your past, what did you do to get here. It is very judgmental. Atkinson did none of that. He said okay we are here now, how do we fix it? He was very future oriented.
Atkinson had designed a long-term program to treat obesity. He explained to his patients that obesity is a chronic disease and they would be in treatment forever. In the first three months of the program, patients would meet several days per week and attend a lecture explaining obesity and the underpinnings of fat. After that, visits decreased to one every one to two weeks, then one every one to two months. Those who started regaining weight were asked to resume more frequent visits. Subjects had to commit to the full program in order to enroll.
Atkinson also introduced Randy to his new postdoctoral assistant, a young scientist from India, Dr. Nikhil Dhurandhar. Dhurandhar examined Randy and studied his blood samples. Randy tested positive for antibodies to Ad-36, meaning he had likely been infected with the virus at some point in the past. Randy remembered being scratched by that rooster as a child, and that afterward his appetite exploded and he started gaining weight quickly. His troubles with food and rapid fat accumulationhe understood it all now. If he was like the chickens, the marmosets, the twins, and the other humans in the study, then his infection with Ad-36 was helping his body to accumulate fat. He says, What Atkinson and Dhurandhar did for me changed my life. They made everything make sense. It was very liberating and very empowering.
How Does a Virus Lead To Fat?
How would a virus like Ad-36 cause fat? Atkinson explains, There are three ways that we think Ad-36 makes people fatter: (1) It increases the uptake of glucose from the blood and converts it to fat; (2) it increases the creation of fat molecules through fatty acid synthase, an enzyme that creates fat; and (3) it enables the creation of more fat cells to hold all the fat by committing stem cells, which can turn into either bone or fat, into fat. So the fat cells that exist are getting bigger, and the body is creating more of them.
The researchers acknowledge that the rooster scratch may have been the start of Randys infection. But they are cautiousthe transmissibility of Ad-36 from chickens to humans has never directly been studied.
Though Dhurandhar and Atkinson have conducted several strong studies showing the contribution of Ad-36 to fatness, skepticism remains. Atkinson says, I remember giving a talk at a conference where I presented 15 different studies in which Ad-36 either caused or was correlated to fatness. At the end of it, a good friend said to me, I just dont believe it. He didnt give a reason; he just didnt believe it. People are really stuck on eating and exercise as the only contributors to fatness. But there is more to it.
Dhurandhar adds, Theres a difference between science and faith. What you believe belongs in faith and not in science. In science you have to go by data. I have faced people who are skeptical, but when I ask them why, they cant pinpoint a specific reason. Science is not about belief, it is about fact. There is a sayingIn God we trust, all others bring data.