In the end, Only Calories Count: Wrong

I’ve been seeing this headline a lot lately:

Diets That Reduce Calories Lead to Weight Loss, Regardless of Carbohydrate, Protein or Fat Content

Well yes that’s true. But quite frankly, it misses the point.

A person who is overweight does not have a weight problem. She has a weight symptom. Her problem is hunger.

There is no point trying to manage weight if you do not manage hunger. There is only so long you can fight your body’s desire to reach and maintain its target weight. And by target I don’t mean the one you have for yourself that makes you look good in a bathing suit. It’s the one your body feels is necessary given your diet composition, your level of activity and your genetic propensity for fat and sugar regulation.
 

Most people don’t know why they are overweight.

They think they know why but they don’t.

The standard answer from patient and doctor alike is “over-eating” which tells you absolutely nothing. I’m here to tell you that there is no such thing as over-eating short of the kind that leaves you feeling unwell because you’ve surpassed the volume comfortable for your stomach.

Over-eating, in the most common sense, refers to any food consumption that precedes weight gain. It’s a tautology. All things being equal, if two people follow the exact same diet and one gains weight, he is said to have “over-eaten” while the other “ate in moderation.” It’s like saying the tree was green because it was green.

The goal of any weight-loss diet should not simply be to create a caloric deficit, but to adopt sustainable lifelong eating habits which make it easy to reach and maintain an ideal weight. That is not to suggest it will ever be easy to drop detrimental eating habits which have been acquired over a lifetime and are probably central to one’s eating culture. But the changes must be sustainable physiologically.

Skinny people may admonish fat ones for failing to show self control, but the fact is that a modern diet makes some people constantly hungry. Fighting that kind of psychological torture day-in day-out is not possible. Gross caloric deficits can be sustained for short periods of time but falling off the wagon is inevitable unless hunger is addressed.

So it is true that the macro-nutrient composition of a diet is irrelevant if you are simply trying to achieve a caloric deficit.

However it is completely relevant if you are trying to control hunger in order to achieve a sustained depletion of fat stores.

Genes remember sugar hit

Just because your blood sugar normalises 8 hours later, it doesn’t mean that cupcake is done with you:

Human genes remember a sugar hit for two weeks, with prolonged poor eating habits capable of permanently altering DNA, Australian research has found.

A team studying the impact of diet on human heart tissue and mice found that cells showed the effects of a one-off sugar hit for a fortnight, by switching off genetic controls designed to protect the body against diabetes and heart disease.

"We now know that chocolate bar you had this morning can have very acute effects, and those effects can continue for up to two weeks," said lead researcher Sam El-Osta, from the Baker IDI Heart and Diabetes Institute.

"These changes continue beyond the meal itself and have the ability to alter natural metabolic responses to diet," he told Australian Associated Press Friday.

Regular poor eating would amplify the effect, said El-Osta, with genetic damage lasting months or years, and potentially passing through bloodlines.

The study’s findings were reported in the Journal of Experimental Medicine.

Source: Yahoo Australia

Recent Research on Metabolism

It’s been a busy week…

New genetic variants that influence fat mass

Fat DNA

 

Half the UK population has the fat “gene”ie “sequence of genes”
…which I affectionately call the “I can’t eat this crap” gene

The sequence they discovered is not a gene, but it sits close to a gene called MC4R, which regulates energy levels in the body by influencing how much we eat and how much energy we expend or conserve. It is thought the sequence might play a role in controlling activity levels of the MC4R gene.

 

Dairy claims false: neither dairy nor calcium intake promotes weight loss

“Our findings demonstrate that increasing dairy product intake does not consistently result in weight or fat loss and may actually have the opposite effect,” the authors conclude.

 

Human metabolic phenotype diversity and its association with diet and blood pressure: Causes Of Disease Can Be Revealed By Metabolic Fingerprinting

Metabolic fingerprinting looks at the relative levels of many different metabolites, which are the products of metabolism, in a person’s blood or urine. Metabolites act as markers which can reveal a lot about how diet and lifestyle contribute to risks for certain diseases.

 

Aspirin-like compounds increase insulin secretion in otherwise healthy obese people

Aspirin-like compounds (salicylates) can claim another health benefit: increasing the amount of insulin produced by otherwise healthy obese people. Obesity is associated with insulin resistance, the first step toward type 2 diabetes.

How is that a benefit? Useful info but bad analysis. Good deconstruction here.

 

I missed this one earlier… Ha! I didn’t see it until it hit the BBC….
Vitamin A, E & Beta-carotene “seem to increase mortality”
I’d love to hear what the stats were on Vitamin D but it wasn’t covered

After various factors were taken into account and a further 20 studies excluded, the researchers linked vitamin A supplements to a 16% increased risk of dying, beta-carotene to a 7% increased risk and vitamin E to a 4% increased risk.

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Short but Long Lived

‘Long-life’ genes found in 100-year-old humans

It’s not quite the elixir of life, but researchers have at last identified gene variants that make people live longer. Men may miss out, as all carriers identified so far are women. They are also slightly shorter than average.

Yes! Finally the odds are tipped in my favour.

short and old

It’s interesting to note the mechanism affected by by the genes.

Both mutations affect the receptor for insulin-like growth factor 1 (IGF1), a driver of bodily growth and maturity, especially during puberty. By making the receptor slightly faulty, the mutations may disrupt IGF1 binding and decelerate the process of maturation and ageing.

Source

Obesity ‘may be largely genetic’

Via the Beeb:

Their American Journal of Clinical Nutrition study found that differences in body mass index and waist size were 77% governed by genes.

It strikes me that a more accurate interpretation is that 77% of obesity can be explained by genetic incompatibility with a modern western diet. Genetics dictates the potential for obesity. Everything else is environmental. Send those people off to the savanna with a sharp stick then get back to me.

It’s not a genetic disease like Tay-Sachs, where the mere presence of the genes equals the disease.
Comment by Mark in What to Eat

If this were not the case, the growing epidemic of obesity would imply that obese people are reproducing more, and are hence “genetically fitter,” than those of normal weight. That may be so but seems unlikely. It also means they are poping out babies like crazy over the past 20 years.

Well if it is true, I would like to report that over the Chinese New Year, I’ve mutated slightly and, due to my genetic make-up, I am larger by 1 pound

Moving On

OK here I am. It seems I’ve really dropped the ball here.

My excuses are the following:

  1. With this blog I set out to answer a question for myself which I think I have answered (more below)
  2. As mentioned previously there are a lot of better blogs out there which cover this topic well.
  3. I’ve come to realise that I have a digital doppelganger already actively blogging.

Last point first. There’s this woman out there who seems to take 12 day holidays when I do, have add-hoc binges and weird sugar lows when I do and even suffers from gastric flu when I do (that was nasty). Plus I gather we are roughly the same weight but for her sake I hope she is taller. OK I don’t get migraines but I do suffer from the occasional bought of tinnitus which I put down to some kind of neural ****ed-upness so there’s that too. So I mean, why bother?

The second point was previously covered

As for the first, I probably need to explain. Scientific truth, as they say, is a function of time. Theories change but we work on the best theory available at the time. If it produces predictable results, then good enough.

So I wanted an answer and at least I have ended up with a working theory. What was my question?

Q: What do I have to do to be my optimal weight (for health, looks, etc) without starving myself or living in a gym. How do I get this fat-ass monkey off my back?

I am now living by a theory that seems to be producing results. It may be naive and historians will trawl through this blog with a chuckle but it works so all critics can just shut the… you know.

The Theory:
I am genetically inclined to store fat when I eat (primarily) wheat products and (secondarily) high GI carbs.
Not everyone has this gene but many do.

OK I appreciate this is hardly an original idea. But whereas it seems a lot of people focus on the short term weight loss possible by a low-carb diet, I am saying that I WILL ALWAYS have these sensitivities and this has to be a permanent dietary change (not withstanding the major slip I had with that corn bread last week).

By simply cutting these foods out and otherwise eating like a pig, my weight has drifted back into what I consider normal ranges (technically I’m still “overweight” with a BMI of 26).

I think that there are other things important for health and longevity (EFAs, certain supplements, weight training and infrequent but intense interval training) but these are not part of “The Theory.” And actually I haven’t been as good about those things as I’d like to claim but my failure hasn’t stopped normalisation of my weight.

I should point out that this is not the only theory I’ve tested over the years but the rest didn’t produce sustainable results.

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OK now that I’ve sorted myself out, does that mean it’s time to go off-line?

Well the truth is that I never really shut up. I have a few other blogs where I put other parts of my life and the chatter is ongoing in the typical jumps and starts which is my way.

But it occurred to me lately that there is still room for reports on the trials and tribulations of living The Theory in the carb paradise known as Asia. And so going forward, while I will not be able to help myself from re-posting goodies I find on this topic, you may find that the blog becomes a bit more anecdotal.

And when I say you, I mean all three of you. Or two. Or perhaps nobody. But anyway I’m happy to talk to myself as there’s nobody else worth talking to around here during the day…

Indians have Fatter Fat

Indian Killer Belly is a strange and scary phenomenon. Asian Indians have a much higher incidence of diabetes and heart disease that other races even when other risk factors have been factored in.

Indian men, no matter where they live, have one of the highest rates of heart disease in the world, even if they have low levels of traditional risk factors such as cholesterol. In fact, even non-smoking vegetarians under 40 who exercise regularly may be at high risk.

While 60 percent of heart attacks amongst Americans occur after age 55, nearly half of all heart attacks among Indian men strike under the age of 55 and 25 percent under the age of 40. Indian women share these high rates of heart disease. Thousands of Indian American men in their 40s and 50s succumb to a first, fatal heart attack every year.

More. Via.

A new study may shed some light on this problem. It seems that Indians’ fat is fatter. Or more precisely, their fat cells are considerably larger than those of caucasians and this is inversely correlated with ability to cope with blood glucose (ie insulin resistance):

Compared to Caucasians, in spite of similar BMI, South Asians had higher total body fat (22±6 and 15±4% of body weight; p-value<0.0001), higher subcutaneous abdominal (SA) fat (3.5±1.9 and 2.2±1.3 kg, respectively; p-value = 0.004), but no differences in intraperitoneal (IP) fat (1.0±0.5 and 1.0±0.7 kg, respectively; p-value = 0.4). SA adipocyte cell size was significantly higher in South Asians (3491±1393 and 1648±864 µm2; p-value = 0.0001) and was inversely correlated with both glucose disposal rate (r-value = −0.57; p-value = 0.0008) and plasma adiponectin concentrations (r-value = −0.71; p-value<0.0001). Adipocyte size differences persisted even when SA was matched between South Asians and Caucasians.

The bottom line is that big fat cells and high levels of subcutaneous fat (but not visceral fat) were found to be risk factors for insulin resistance and heart disease. More.

Health warning: the innocence of visceral fat is not supported by other studies. Also, this study only included a total of 29 south Asians and 19 Caucasians. More research is needed.

Single Gene Controls Body Fat

A gene found in many animals – from fruit flies to humans – has been shown to regulate fat synthesis and storage:

Mice with [the fat burn gene switched off] ate as much or more than normal mice. However, they were leaner, had diabetes-resistant fat cells, and were better able to control insulin and blood-sugar metabolism. In contrast, animals with [the fat burn gene turned down] were fatter and less healthy, and had diabetes. The researchers also showed that gene activity could be turned up or down, not just on or off.

So is a “I can remain on the couch and yet be a babe” pill in the works? Don’t hold your breath.

Dr David Haslam, clinical director of the National Obesity Forum, warned that it could take many years to develop genetic treatments for obesity. In the meantime, he said, the only way to tackle the problem effectively was to encourage people to eat healthily and take exercise.

More at the BBC.

Hunting Longevity Genes

People who live to 100 or more are known to have just as many—and sometimes even more—harmful gene variants compared with younger people. Now, scientists at the Albert Einstein College of Medicine of Yeshiva University have discovered the secret behind this paradox: favorable “longevity” genes that protect very old people from the bad genes’ harmful effects. More

 

 

Fat? I’ve just got big genes

The Times Online does a run down on some of the reasons that you are fat… that are not your fault.

First – Genetics:

People who inherit one version of the FTO gene rather than another are 70 per cent more likely to be obese, and weigh an average of 3kg more.

Next – Pathogens

A study at Louisiana State University (LSU) showed that exposure to adenovirus36 (Ad36), which normally causes coughs and colds, can induce stem cells from fat tissue to become fully fledged fat cells. Though the findings applied only in the laboratory, they matched observations that 30 per cent of obese people carry the virus, compared with only 11 per cent of the lean. (…)

Two other adenoviruses have been linked to weight gain…

But the author concludes by pointing out that, by and large, being obese is ultimately the responsibility of the individual

For the vast majority of people – genetically predisposed, virally infected or not – a simple equation still applies. Consume more calories than you burn off and you will put on weight.

Full Article