The fight is on over sugar

ScientistIt is difficult even for experienced scientists to agree on the interpretation of their findings. Add to that external research funding linked to commercial interests and it is even more difficult to know what to believe.

A case in point. If you thought excessive sugar intake is the root of the evil obesity epidemic you might have to think again.

Or not….

Sugar advice questioned

There has been a scathing attack on global health advice to eat less sugar. Through industry proxies, a scientific review now claims that warnings to cut sugar are based on weak evidence and cannot be trusted.

The review identified 9 guidelines that offered 12 recommendations, all indicating a suggested decrease in the consumption of foods containing nonintrinsic sugars (that is added sugar to you and me). The recommendations were based on various health concerns, including nutrient displacement, dental caries, and weight gain. However, the reviewers claimed that no guideline met criteria for trustworthy recommendations and were all based on low-quality evidence.

The review was paid for by the International Life Sciences Institute, a scientific group funded by multinational food and agrochemical companies.

Tainted from the beginning. When will industry ever learn.

The review findings immediately questioned

Predictably, the review quickly received sharp criticism from public health experts. It was but the latest effort of the food industry to influence global nutrition advice by supporting prominent academics questioning the role of sugary food and beverages in causing obesity and other health problems.

The review was seen as an attempt to undermine sugar guidelines from the World Health Organization (WHO) to consume fewer products with added sugar, such as soft drinks, candy and sweetened cereals. It is a classic example of how industry funding is used to influence opinion.

To be fair to the review team, they wanted their results to be used to promote improvement in the development of trustworthy guidelines on sugar intake. They also emphasised that the review findings should not be used to justify higher intake of sugary foods and beverages.

Still, nutrition experts say that the review team ignored the hundreds of randomised controlled trials that have documented the harms of sugar. There are strong scientific evidence that sugar contribute to adverse health conditions like weight gain and Type 2 diabetes. The view is that the review team ignored the real data, created false scores, and somehow got through a peer review system difficult to understand from a reputable journal like Annals of Internal Medicine.

The WHO contrary point of view


So until we have the general scientific opinion swinging over to supporting sugar, it is clearly best to stick to the WHO recommendations.

A WHO guideline of 2015 recommends that adults and children reduce their daily intake of free sugars to less than 10% of their total energy intake. WHO also believes that a further reduction to below 5% or roughly 25 grams (6 teaspoons) per day would provide additional health benefits.

Free sugars refer to monosaccharides (such as glucose, fructose) and disaccharides (such as sucrose or table sugar) added to foods and drinks by the manufacturer, cook or consumer, and sugars naturally present in honey, syrups, fruit juices and fruit juice concentrates. But the guideline does not refer to the sugars in fresh fruits and vegetables, and sugars naturally present in milk.

Contrary to the above review findings, WHO states that they have solid evidence that keeping intake of free sugars to less than 10% of total energy intake reduces the risk of overweight, obesity and tooth decay. Based on the quality of supporting evidence, these recommendations are ranked by WHO as “strong”.

So there you have it. And if you embark on reducing your sugar intake remember that much of the sugars consumed today are “hidden” in processed foods that are not usually seen as sweets.

Magical dietary fibres


Dietary fibre can influence appetite (Photo: Tony Evans).

We have all heard the “eat more fibre” mantra and wondered what this is all about. So did scientists. Sure we have long known it is good for gut health and function. Recently with the exploration of the gut microbes – the microbiota – we have learnt that dietary fibre can support survival and growth of the good bugs. That we have written about before.

Now scientists have found another piece of the puzzle. Some of the fermentation products produced by the gut microbes from the dietary fibre that our own enzymes cannot digest have the potential to influence our appetite. That is incredible and provides a further insight into the obesity conundrum.

The new mechanism

Obesity is currently one of the most serious global threats to human health. Susceptibility to obesity is determined by genetic background, diet, and lifestyle. Now it has become apparent that the resident intestinal microbes in the large intestine also play an important role.  During the process of microbial fermentation of non-digestible fibre, the short-chain fatty acids acetate, propionate and butyrate are formed.

While short-chain fatty acids can serve as an energy source, the scientists showed that they also act as signaling molecules for the free fatty acid receptor 2 (FFAR2) found in enteroendocrine L cells in the large intestine. These specialised gut cells secrete the appetite suppressing hormone peptide YY (PYY). FFAR2 signaling was found to drive an expansion of the PYY cell population within the large intestine, leading to increased circulating PYY. This is associated with a reduction in food intake and protection against diet-induced obesity.

Evidence points to the production of short-chain fatty acids by the gut microbiota as an important appetite regulatory signal.

So what are fibres?


Almonds are good sources of dietary fibre.

Just to be clear, dietary fibre is the indigestible portion of food derived from plants. Chemically, dietary fibre consists of non-starch polysaccharides such as arabinoxylans, cellulose, and many other plant components such as resistant starch, resistant dextrins, inulin, lignin, chitins, pectins, beta-glucans, and oligosaccharides. Food sources of dietary fibre are often divided according to whether they provide predominantly soluble or insoluble fibre.

Soluble fibre is found in varying quantities in all plant foods, including in a range of legumes, in oats, rye, chia, and barley, in several fruits, in vegetables, in root tubers and in nuts, with almonds being the highest in dietary fibre.

Sources of insoluble fiber include whole grain foods, wheat and corn bran, legumes such as beans and peas, nuts and seeds and vegetables such as green beans, cauliflower, zucchini and celery.

So there you have a wide variety of healthy foods with the potential of reducing your hunger pangs and alleviate the risk of overweight and obesity.

New bad findings for bisphenol A

Canned food

Bisphenol A can be found in many canned food products.

We have covered bisphenol A, called BPA for short, several times before. In case you need to be reminded, it is a chemical widely used in plastic water bottles, metal food cans, and receipt paper. A large number of scientific publications have questioned the safety of BPA. High doses were found to influence the hormonal balance by acting as an endocrine disruptor with oestrogenic effects already in the 1930’s.

Debate over the toxicity of BPA is on-going with findings of potential low-dose effects particularly worrying. The European Food Safety Authority (EFSA) has so far refrained from suggesting that BPA should be banned, contrary to the opinion of government scientists from France and Denmark. At least EFSA lowered the temporary tolerable daily intake (tTDI) by more than 10 times in its latest opinion. And BPA has been removed from baby bottles in many countries.

New bad reports piling up

By setting a temporary TDI, EFSA committed to the re-evaluation of BPA when a two-year study by the U.S. National Toxicology Program becomes available in 2017. But in the meantime results from several other studies have been published.

A report by the Dutch National Institute for Public Health and the Environment (RIVM), critically examined two studies describing pre- and perinatal effects of BPA on the immune system. The report recommended supporting research on alternatives to BPA and advising consumers to reduce their exposure to BPA from food and other sources.


Foetal exposure to BPA promotes obesity later in life for girls.

And another recent study equally points to the often neglected prenatal exposure to BPA. A team of U.S. researchers tracked 369 mother-child pairs from the third trimester of pregnancy until the children turned seven years old. They measured BPA levels in the mothers’ urine during pregnancy and then checked the children’s height, weight, waist circumference, and body fat as they aged, also measuring their BPA levels. They adjusted the results for factors that could potentially skew the results, including race and pre-pregnancy obesity among the mothers.

They found that the higher the mothers’ BPA exposure was during pregnancy, the more signs of obesity girls showed at age seven. There was no such association for boys; nor was there any relation between BPA levels in the children’s urine and obesity as they grew.

So it seems that the foetal period is when we’re most vulnerable to BPA and its ability to alter metabolism and the way our bodies generate fat cells. It is not surprising that BPA seems to affect girls differently than boys since as an endocrine-disrupting chemical it mimics or blocks hormones produced by the body. Boys and girls produce different hormones, so hormone-disrupting chemicals might be expected to affect them differently.

And if that’s not enough, experimental laboratory evidence suggests that BPA is a neurodevelopmental toxicant. In further disturbing findings, a longitudinal cohort study confirmed the association between prenatal BPA exposure and child behaviour in preschool-age children, accounting for postnatal BPA and other potential confounders. Among boys, prenatal BPA exposure was positively associated with higher scores on all syndromes and significantly associated with Emotionally Reactive and Aggressive Behaviour. Inverse associations were seen in girls for all syndromes and these associations were significant for Anxious/Depressed and Aggressive Behaviour.

How long to wait?

Protect your child from becoming obese.

Take your own action to protect your child from becoming obese.

So it seems pretty clear that BPA can have significant effects at levels of exposure seen in real life.

Do we really have to wait further for some real progress. Authorities seem reluctant to take decisive action despite overwhelming proof of harmful effects. Sure, not all findings point in the same direction and alternatives to BPA might be as bad.

But don’t despair, you can take your own action. To reduce exposure to BPA, the National Institute of Environmental Health Sciences recommends avoiding plastic containers numbers 3 and 7, shifting from canned foods to fresh or frozen foods, and, when possible, choosing glass, porcelain, or stainless steel containers, especially for hot food and liquids.

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Lead – up to no good


Lead in petrol an earlier culprit in lead poisoning.

Lead has been used for thousands of years because it is widespread, easy to extract, and easy to work with. It is highly malleable and easily meltable. Equally, lead poisoning has been documented since ancient Rome, ancient Greece and ancient China. It is thus clear that, ingested or inhaled, lead is poisonous to animals and humans. Still we were foolish enough to add it to petrol starting in the 1920s and use lead pigments particularly in white but also in yellow, orange, and red paint to spread its occurrence even further.

We have lived with the consequences ever since. Lead poisoning typically results from ingestion of food or water contaminated with lead, but may also occur after accidental ingestion of contaminated soil, dust, or lead-based paint. It is a neurotoxin that accumulates both in soft tissues and the bones, damaging the nervous system and causing brain disorders. Lead has been shown many times to permanently reduce the cognitive capacity of children at extremely low levels of exposure. Lead exposure in early childhood has also been linked to violent crime.

But there is more

As if that was not enough, new research has shown that early life exposure can alter the composition of the gut microbiota (remember one of my favourite topics), increasing the chances for obesity in adulthood. So far at least in mice. Lead was added to the drinking water of female mice prior to breeding through nursing their young. The lead levels used  were designed to be within past and present human population exposure levels. Thus the lowest dose used of 5 µg/dL is the same as the current US blood lead action level, while the higher dose mirrored exposure levels during the 1960s and 1970s to be able to evaluate both current and historically relevant lead levels.

Once weaned, the offspring were raised to adulthood without additional exposure, and then tested for lead effects acquired from their mothers. The guts of both males and females exposed to lead had all of the similar complexity in microbiota as those not exposed. The differences were in the balance of the different groups of microorganisms. Due to differences in their gut microbiota, adult male mice exposed to lead during gestation and lactation were 11 percent heavier than those not exposed. But not females, although the researchers speculate that females might have shown effects on obesity if they had followed them longer.

Although improving, it is not over yet


Lead exposure linked to obesity in mice.

So now we have obesity added to the long list of potential harm caused by lead contamination. Fortunately, by the mid-1980s, a significant shift in lead end-use patterns had taken place with lead use phased out from petrol in many countries and banned from paint, but still remaining in some grades of aviation fuel, and in some developing countries.

Although the situation has improved, it is not over yet. Lead may be introduced to foods from the use of lead containing pottery or lead crystalware. Another source is water from lead containing pipes. And wild game that has been shot with lead pellets. Not to forget some odd Chinese herbs found to contain high lead levels.

So vigilance is still needed.

Leptin undercover activities

Leptin and cardiovascular disease (Photo: Gabriela Camerotti)

Leptin and cardiovascular disease (Photo: Gabriela Camerotti)

In a previous post we discussed the beneficial effects of leptin, the satiety hormone, in normal weight individuals. Leptin, produced by fat cells, tells the brain when we should stop eating. Makes sense.

More problematic is the situation in obese individuals where the leptin feed-back on food intake has stopped working.

If that wasn’t enough, it gets even worse. While high levels of leptin don’t help obese individuals lose weight, new research even show that they can directly contribute to cardiovascular disease.

A double whammy

It seems ironic that fat makes leptin, but obese individuals with excessive fat accumulation become insensitive to leptin’s impact on their metabolic, but not their cardiovascular system. Exactly why leptin cannot tell our brain to stop eating, but it can still tell the body to increase the activity of the cardiovascular system is a conundrum.

At least new research findings have explained the second part of the equation. In both cell culture and animal models, the researchers have shown that leptin directly activates aldosterone synthase expression in the adrenal glands, resulting in production of more of the steroid hormone aldosterone. That is not good.

High aldosterone levels are known to contribute to widespread inflammation, blood vessel stiffness and scarring, enlargement and stiffness of the heart and impaired insulin sensitivity. It also has a direct effect on blood pressure by regulating salt-water balance in the body. But exactly how it got high in obesity was a mystery.

Possible treatment on the way

Results so far from mice (Photo: Wikimedia)

Results so far from mice (Photo: Wikimedia)

Identifying the direct connection of high levels of leptin and aldosterone is a break-through in understanding the cause of the increased cardiovascular disease  risk in obese individuals. So far only in mice, but early results from human trials show the same correlation, and strongest in females, who make much more leptin.

There are already existing drugs that could work to ameliorate the situation, including an old blood pressure drug, spironolactone, that directly targets aldosterone activity. Spironolactone, a diuretic, helps the kidney eliminate water and sodium but hold onto valuable potassium. It works by blocking the receptor to which aldosterone binds.

There are also leptin receptor blockers under study for a wide range of problems from obesity to cancer.

So better know your leptin undercover activities to keep healthy.

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The complexity of weight gain

No fatness gene found.

New fatness gene found.

They have found the culprit, the fatness gene. So all we need now is a bit of gene therapy, or not. Still feel hungry? Well, there is an explanation for that as well. Or is it the carbohydrates that are responsible for the explosion of obesity. According to the latest diet advice you should avoid all kinds of carbs, but eat as much fat as you like. Previously it was the fat to avoid, with a proliferation of low-fat products that now seem redundant. But the Coca-Cola Company and its ilk wouldn’t give up their sugary drinks that easily. They have enlisted a number of fitness experts to promote exercise as the solution. Sounds complex? Well, that is because it is. Let’s look at the ideas one at a time.


We have to start with hunger. Have you ever heard of the AGRP neurons? I guess not, but if you’re often hungry you can blame hunger-sensitive cells in your brain known as AGRP neurons. These neurons are responsible for the unpleasant feelings of hunger making sure that you look for food when your energy level is low, even if you don’t want to. They seem to be an evolutionary part of a motivational system to encourage ancient humans to seek food or water despite having to venture into dangerous environments to do so. Their signals should really be redundant now when food is readily available, but they remain, making it a struggle to maintain a restricted diet and lose weight.

In earlier studies, researchers found that other neurons that promoted eating did so by increasing positive feelings associated with food. In other words hunger makes food taste better, which seems natural. On the contrary the AGRP neurons produce negative feelings. Surprisingly, research results using mice showed that they did not actually have to eat to quiet the AGRP neurons. Instead, the cells ceased activity as soon as an animal saw food or even an artificial signal that predicted food. And their activity remained low while the animal was eating.

If you think that you can just look at food to relieve hunger pangs, think again. Unfortunately, other neurons will make sure that you also eat the food. So no luck there.

Fatness gene

Moving on from the brain to the genome. Scientists have previously found over 100 regions on the human genome that correlate with obesity, likely through regulating the brain’s perception of hunger (here we go again) and the distribution of fat throughout the body. Now scientists at the University of British Columbia have discovered a gene that directly controls the production of fat cells and the growth of those cells, which are precursors to obesity.

The gene can be found in every cell of the body and encodes a protein called 14-3-3zeta. Silencing the gene in mice resulted in a 50 per cent reduction in the amount of unhealthy white fat that is associated with obesity, heart disease and diabetes. And this was despite the mice consuming the same amount of food. The scientists not only identified zeta as the operative protein, but demonstrated a clear cause-and-effect between 14-3-3zeta and fat accumulation.

We get fatter through the multiplication of our fat cells, and through the growth of individual fat cells. And the zeta protein affects both the number of cells and play a role in the growth cycle of these cells. Early days yet, but scientists speculate that there could be possible to suppress the gene or to develop a drug that could block the protein and thus prevent fat accumulation in people who are on their way to become overweight.

But there is a large gap between theory and practice, so no luck yet.

Fat and carbs

Low-fat food popularity (Photo: Barry Ennor).

Low-fat food gained popularity (Photo: Barry Ennor).

So what can you do now? Let’s look at the two individual components of the diet that have been associated with weight gain. A lot of people have very strong opinions about what matters for weight gain, as we have covered before. First it was fat as it seems natural to associate fat consumption with fat accumulation. And fat also provides double the energy per weight compared to the other macro nutrients. Thus industry developed a number of low-fat products to entice consumers. However, they still wanted the products to taste good so in many cases they increased the sugar content and thus energy intake. Such products have been popular for quite some time, but our metabolism is complex so in reality people didn’t really lose weight. Out came the carbohydrate theory, proposing instead that it was carbs that made us fat and not fat in the diet. So fat became free for all but carbohydrate-rich sources like bread, pasta and potatoes should be limited as much as possible. And people on such diets actually lost weight.

So is it proven? Hold on, not so fast. A new study from the US National Institutes of Health presents some of the most precise human data yet on whether cutting carbs or fat has the most benefits for losing body fat. And the researchers show how, contrary to popular claims, restricting dietary fat can lead to greater body fat loss than carb restriction, even though a low-carb diet reduces insulin and increases fat burning.

Despite authoritative claims about carbohydrate versus fat restriction for weight loss, nobody had ever measured in detail what would happen if carbs were selectively cut from the diet while fat remained at a baseline or vice versa. Studying the effects of diet on weight loss is often confounded by the difficulty in measuring what people actually eat. To counter this, 19 consenting adults with obesity were confined to a metabolic ward for a pair of 2-week periods, over the course of which every bit of food eaten was closely monitored and controlled. During the first period, 30 per cent of baseline calories were cut through carb restriction alone, while fat intake remained the same. During the second period the conditions were reversed.

At the end of the experiment body fat lost with dietary fat restriction was greater compared with carbohydrate restriction, even though more fat was burned with the low-carb diet. However, over prolonged periods the model predicted that the body acts to minimize body fat differences between diets that are equal in calories but varying widely in their ratio of carbohydrate to fat. So the conclusion is that although not all calories are created equal when it comes to body fat loss, over the long term, it’s pretty close.

So feel free to limit energy intake the way you feel most comfortable with, as long as it is consistent over time.


Exercise not enough to reduce weight (Photo: Sangudo).

Exercise not enough to reduce weight (Photo: Sangudo).

The remaining part of the energy equation is energy expenditure. Coca-Cola, the world’s largest producer of sugary beverages, is backing a new “science-based” solution to the obesity crisis: Exercise more and worry less about cutting calories to maintain a healthy weight.

The beverage giant provides support to a new nonprofit organization called the Global Energy Balance Network with a team of influential scientists who are promoting the message in medical journals, at conferences and through social media. And the message:  Weight-conscious consumers are overly fixated on how much they eat and drink while not paying enough attention to exercise.

This message has not been uncontested with health experts saying it is misleading and an effort to deflect criticism about the role sugary drinks have played in the spread of obesity and Type 2 diabetes. It is clear that exercise has only minimal impact on weight compared with what people consume. A food industry critic, professor Marion Nestle, is especially blunt in her comments: The Global Energy Balance Network is nothing but a front group for Coca-Cola. Coca-Cola’s agenda here is very clear. Get these researchers to confuse the science and deflect attention from dietary intake.

While people can lose weight in several ways, many studies suggest that those who keep it off for good consume fewer calories. Growing evidence also suggests that maintaining weight loss is easier when people limit their intake of high glycemic foods such as sugary drinks and other refined carbohydrates, which sharply raise blood sugar.

So what to do?

There is nothing much you can do yet about the genes you have inherited from your parents. But you can make sure that you eat a nutrient dense diet rather that an energy dense diet, and reduce overall energy intake in a way you feel comfortable with. As scientists say about their studies, rubbish in, rubbish out, or in this case junk food in, belt out. Physical activity is important and certainly helps. But studies show that exercise increases appetite, causing people to consume more calories. Exercise also expends far fewer calories than most people think. And to compensate the fluid loss with an energy drink at the end of the exercise completely defeats the purpose.

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The pervasive obesity curse

Obese (Photo: Malingering)

Excess body weight an increasing problem (Photo: Malingering)

Excess body weight is a major individual, societal and economic problem as it is spreading globally, still increasing rapidly, and can have many and varied health consequences. In its more severe forms, obesity places huge financial burdens on governments and individuals and has been reported to account for up to six per cent of total health care costs in some developed countries.

There is a negative stigma attached to overweight and obesity and a high public awareness of the associated health risks as reflected in a wealth of dietary advice published almost daily. Public health campaigns have long warned against excess body fat and promoted messages highlighting the importance of a healthy diet and moderate exercise. Yet it is a conundrum that much of current prevention strategies for limiting weight gain seems to be simply ignored by individuals and society alike. Individuals continuously make choices in their everyday life to evade a multitude of risks, but excess weight gain seems not to be prioritised. Society continues to provide tempting food choices and facilitates sedentary lifestyles. Intensive promotion of energy-dense food and drink to children and adults has created a new food model of convenience. The structure of the built environment affects obesity by restricting physical activity.

In its simplest form it is clear that excess weight gain is caused by an imbalance between an individual’s energy consumed and energy spent, acknowledging genetic differences in metabolic rate. Obesity could be seen as an unintended consequence of affluence leading to overindulgence, a sedentary lifestyle and bad food choices by the individual. However, it is now commonly agreed that the reasons for the growth in overweight and obesity are multifactorial. Instead of seeing it as a weakness of the individual, it makes much more sense to view obesity as a societal problem involving the interaction of the individual with what has been called the “obesogenic” society.

Fast food contributing to weight gain (Photo: Tony Evans)

Fast food contributing to weight gain (Photo: Tony Evans)

The twenty-first century is a fast moving society where multitasking and food convenience are promoted. Time has become increasingly precious and fast food that can provide satiety in the shortest time possible has become the norm in an increasing number of societies. Globally, the availability of energy-dense and refined foods for easy consumption, foods often high in fat and sugar, have led to excessive energy intake. Sugar and fat are powerful sources of neurobiological rewards. Energy-dense foods provide more sensory enjoyment and more pleasure.

Fast food has become synonymous with time efficiency and has become a middle class status symbol of efficiency in poor countries. But fast food has also, because of its success, become food that is low in price and affordable for people on low income and the poor in rich countries.

It is time for an overall system change. We need to rethink the way we design cities and make them conducive to a healthy lifestyle. Healthcare systems should focus more on prevention and primary care. We need to reconnect with food and teach food skills to young people. We need to take back our urban environment and stop letting it become an advertising space for food and drink companies selling unhealthy choices. Without decisive action, overweight and obesity might become the new normal.

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Even more vegetables


We should eat more fruit and vegetables

The World Health Organisation advised in 1990 that the minimum daily intake of fruit and vegetables should be 400 g a day, but note that this excludes consumption of potatoes and other starchy tubers. The aim was to prevent chronic diseases such as heart disease, cancer, diabetes and obesity, and to reduce several micronutrient deficiencies, especially in less developed countries.  To promote the recommendations, WHO and FAO started a joint worldwide initiative in 2003.

But what exactly we should eat is not so easy. The definition of the word vegetable is somewhat arbitrary and subjective. All parts of herbaceous plants eaten as food by humans are normally considered vegetables. Mushrooms, actually belonging to the biological kingdom fungi, are also commonly considered vegetables. Potatoes and other starchy tubers are included in the definition of vegetables in some countries but not in others, which is not that helpful. Nuts, grains, herbs, spices and culinary fruits are normally not considered as vegetables. Botanically, fruits are reproductive organs, while vegetables are vegetative organs which sustain the plant. Nevertheless, several fruits, e.g. cucumbers and tomatoes, are also included in the term vegetables.


A formal definition of fruits and vegetables by the World Health Organisation might help:

Fruit and vegetables are edible plant foods excluding cereal grains, nuts, seeds, tea leaves, coffee beans, cocoa beans, herbs and spices.

Fruits are edible parts of plants that contain the seeds and pulpy surrounding tissue; have a sweet or tart taste; generally consumed as breakfast beverages, breakfast and lunch side-dishes, snacks or desserts.

Vegetables are edible plant parts including stems and stalks, roots, tubers, bulbs, leaves, flowers, and fruits; usually include seaweed and sweet corn; may or may not include pulses or mushrooms; generally consumed raw or cooked with a main dish, in a mixed dish, as an appetiser, or in a salad.

Are you with me so far?

Now some countries have attempted to translate this into portions to help your calculations.

In the United Kingdom the recommendation is to eat five fruit and vegetable portions a day with each portion equivalent to 80 g. However, only about 30% of the population manage to consume the recommended amount.

Australia went one step further and recommends two fruit and five to six vegetable portions a day with the fruit portion at 150 g and vegetable portion at 75 g. This equates to an enormous total of 675 to 750 g. Quite an ambitious target. Close to 50% of Australians reported that they usually ate two or more serves of fruit per day, while 8% usually ate five or more serves of vegetables per day. Taking both guidelines into account, only 5.5% of Australian adults had an adequate usual daily intake of fruit and vegetables.

Canada previously recommended five to ten portions for all, but changed this in 2007 to specific recommendations for each age and sex group. They now recommend a minimum of four portions for young children up to a minimum of eight portions for adult males. Only 26% of the population aged 2 years and older consumed the minimum number of daily servings recommended for their respective age–sex group.

France and Germany also recommend five portions a day while portion numbers vary in other European countries. The United States abandoned the numbers in favour of a generic fruit and vegetable campaign in 2007 indicating that the more you eat the better it is. In Europe, the average consumption of fruit and vegetables is only 220 g per person per day and just 27% of European mothers consume over 400 g. The French did not reach the recommended amounts consuming fruit only 1.3 times per day and vegetables 2.3 times per day despite all the talk about the beneficial Mediterranean diet. Still this was better than the Americans. Adults in the United States consume fruit about 1.1 times per day and vegetables about 1.6 times per day. That is definitely on the low side but not breaking any non-existent recommendations.

Given our notorious dishonesty when confronted by pollsters with questions that touch on our self-regard, there might even be a lot less five-a-day eaters than indicated above.

But if you are struggling with reaching the current recommendations just wait for it.

A new study, carried out by researchers at University College London, analysed information from more than 65,000 adults aged 35 years or older, who responded to the Health Survey for England. Researchers then followed up participants for an average of 7.7 years after their initial participation. The study found that people who ate seven or more portions of fruit or vegetables a day had a 33% reduced risk of death from any cause, a 25% reduced risk of death from cancer and a 31% reduced risk of death from cardiovascular disease, compared with people who ate less than one portion per day.

Not even 400 g is enough

Not even 400 g is enough (Chris Walton)

So not even five portions of fruit and vegetables a day may, after all, be enough. There was a surprise finding – eating canned or frozen fruit actually may not be helpful at all. This is a little confusing but it could be that people eating canned fruit may not live in areas where there is fresh fruit in the shops, which could indicate a poorer diet. And merging canned and frozen fruit might not be fair to the frozen produce.

The clear finding was that eating more fresh fruit and vegetables, including salads, was linked to living a longer life generally and in particular, to a lower chance of death from heart disease, stroke and cancer. Vegetables seemed to be significantly more protection against disease than eating fruit.

The researchers commended the Australian example as the one to follow where the balance is two fruit and five vegetables. That is if the reduced risk of disease is entirely attributable to fruit and vegetable consumption, or they are acting as a marker of a broader dietary pattern associated with improved health.

Your call, but to up your fruit and vegetable consumption to close to 800 g a day might not be easy.

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Energy burning brown fat

The painful way of forming brown fat (Photo: Pavel Trebukov)

The painful way of forming brown fat (Photo: Pavel Trebukov)

You’re out there freezing (assuming you live in the Northern Hemisphere, here in Australia it’s summer). You’re shivering and actually feel some warmth. It is your muscles burning off energy to warm you up a little bit. But what you don’t know is that at the same time the muscles release irisin. The irisin goes straight to your white fat cells and some are gradually transformed into brown fat cells and activated. And the brown fat cells burn energy rather than storing it relieving the muscles from some shivering activity. Clever don’t you think?

Some puzzling findings

But let’s take a step back. Babies are actually born with a supply of brown fat in the neck region. This is nature’s way of helping infants to keep warm by burning energy when needed. When growing up the brown fat disappears. Or so it was thought. But brown fat has been rediscovered in adulthood in the same neck region. Now a new study suggests that shivering and moderate exercise are equally capable of stimulating the conversion of energy-storing white fat into energy-burning brown fat. Around 50 g of white fat stores more than 300 kilocalories of energy. The same amount of brown fat could burn up to 300 kilocalories a day. Quite a difference. There are a few puzzling findings here. It makes sense for shivering to produce and activate brown fat to help in the process of keeping warm. But the communication between muscle and fat through the irisin hormone to achieve this is quite astonishing. Even more surprising is the fact that exercise can achieve the same result. It is not intuitive since exercise produces heat. It is speculated that muscle contractions during exercising mimic shivering and thus achieve a similar effect. The scientists found that around 10-15 minutes of shivering resulted in equivalent rises in irisin as an hour of moderate exercise. Just be aware that it might take up to a week for the brown fat to be fully developed.

The facts about brown fat

The less painful way of forming brown fat (Photo: Steve Garner)

The less painful way of forming brown fat (Photo: Steve Garner)

We now know that brown fat is present in most, if not all, adults. Adults with more brown fat are slimmer than those without. When we are cold, we first activate our brown fat because it burns energy and releases heat to protect us. When that energy is insufficient, muscle contracts to produce shivering, thereby generating further heat. The brown fat can provide around 20% of the heat needed, representing a proportion of total energy expenditure sufficient to impact the body’s long-term energy balance. There is excitement in the brown fat field because its energy-burning capacity makes it a potential target to combat obesity. Glucose levels are also lower in humans with more brown fat, potentially providing protection against diabetes.

Your daily treat

So there you have the food connection. As long as you regularly exercise for about an hour or, if you prefer, spend 10-15 minutes in a cold room at 12-14˚C you can have your daily ice cream without putting on weight. I know what I prefer to do.

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Slimming during your sleep

Losing weight during sleep (Photo: RelaxingMusic)

Losing weight during sleep (Photo: RelaxingMusic)

When you go to bed and close your eyes you might start a process of losing weight. It is really contrary to what you would believe. The normal theory is if energy in through food exceeds energy out through exercise you will gain weight. And during sleep you don’t get much exercise unless you are sleep-walking. But read on and you will learn what a little cold and the very small pineal gland can do to your body.

The pineal gland, or the “third eye” as it has sometimes been called, is a small endocrine gland situated in the  brain. Its shape resembles a tiny pine cone, hence its usual name. It seems to have acted as a light sensitive eye in some ancient animals and still does in a few surviving species like the lamprey, thus the naming as the third eye. As a matter of fact light still regulates its activity. Light signals are sent from photosensitive cells in our eyes and through a brain pathway to the pineal gland that in turn regulates our circadian rhythm that is so vital to proper sleep. It does this by producing melatonin during the night since the production of melatonin is stimulated by darkness but inhibited by light.

The illusive brown fat

Now we have to look at brown fat to complete the story. Brown fat is one of two types of fat found in mammals. The other type is the normal white fat that we only use for energy storage. However, the primary function of brown fat is not to store energy but to generate body heat. This is vital to newborn babies that cannot shiver and it makes up about 5% of their body mass. It is located on the back, along the upper half of the spine and toward the shoulders. Brown fat cells are actually more related to muscle cells than to white fat cells in that they carry a much higher number of iron-containing mitochondria, the energy machines of our cells, and more capillaries to supply their greater oxygen needs. Both factors that create the brown colour.

The brown fat will decrease with age and was initially believed to be almost non existent in adults. However, new imaging technologies have found small amounts in the neck, upper back, and clavicles of adults.  Aside from knowledge of its anatomic presence, little was known about the role of brown fat in adults until the past few years. Now, new research has shown that it also can contribute to regulating body temperature in adults in that this highly metabolically active tissue will burn energy to generate heat when we are exposed to cold temperatures. Dutch researchers subjected a group of people to a 15-16 ºC temperature for 6 hours per day and found that the brown fat increased its metabolic activity and became more efficient in keeping us warm. Similarly, Japanese researchers exposed healthy human subjects to cold and found an increase in brown fat activity and energy expenditure, and a decrease in body fat mass at the end of the study. The authors of both the Dutch and Japanese studies concluded that regular exposure to colder temperatures could be effective in reducing the prevalence of obesity in the population.

Melatonin an alternative to cold

Being cold is not everyones cup of tea (Photo: ObertoMaidelys)

Being cold is not everyones cup of tea (Photo: ObertoMaidelys)

Now we might not like to spend time in cold temperatures to lose body weight, but, you guessed it, the pineal gland comes to the rescue. Apart from regulating the circadian rhythm, melatonin is also involved in energy metabolism and body weight control. Melatonin promotes the recruitment of brown fat cells and enhances their activity, thus raising the body’s basal metabolic rate. And there is more. Spanish scientists have an explanation to the puzzling conundrum of the effect melatonin has in countering obesity. They found that melatonin can transform white fat to beige fat, a structure with similar effects to brown fat. While white fat stores calories leading to weight gain, beige fat helps regulate body weight by burning calories.

So a good night’s sleep might stimulate your melatonin production and help you lose weight. If you’re a light sleeper you might be happy to know that melatonin can also be found in fruit and vegetables like mustard, Goji berries, almonds, sunflower seeds, cardamom, fennel, coriander and cherries. Sleeping in the dark and consuming the right fruit and vegetables could help control weight gain and prevent cardiovascular diseases associated with obesity. And why not the occasional stay in a cold environment. There are melatonin pills available as well for the lazy. And just before you go overboard with your sleep patterns, you should know that some of the data come from animal experiments and will still need to be confirmed in humans. But why destroy a good story?

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