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Fat accumulation is determined not by the balance of calories consumed and expended but by the effect of specific nutrients on the hormonal regulation of fat metabolism. Obesity is a condition where the body prioritizes the storage of fat rather than the utilization of fat.
Insulin is the most important hormone in our body when it comes to fat mobilization (breakdown) and fat storage. This is a fact. There is not one person who studies the endocrine system who will not acknowledge the following quote from Lehninger’s Principles of Biochemistry (the “bible” of biochemistry).
“High blood glucose elicits the release of insulin, which speeds the uptake of glucose by tissues and favors the storage of fuels as glycogen and triglycerides, while inhibiting fatty acid mobilization in adipose tissue.”
In other words, eating glucose (carbohydrates) increases insulin levels in our body. Insulin drives glucose into liver and muscle cells as glycogen (in small, finite amounts) and into fat cells as triglycerides (in unlimited amounts). Insulin also inhibits the breakdown and utilization of fat, as shown here.
Insulin does not act alone, and the story of fat storage and breakdown is complex if you want to understand every single detail, but the “first order term” is insulin. I will spend time in the future writing about insulin’s “dance partner,” leptin. But insulin is probably the General when it comes to determining how the body partitions fat.
So, insulin is sort of like gravity. It’s in your body whether you know about it or not. It’s acting on your cells whether you like it or not. It’s playing a major role in determining your ability to mobilize versus store fat if you believe me or not.
Does this mean insulin has the same effect on everyone? Does this mean insulin has the same effect on any given person over time? Of course not. Contrast me and my wife. I look at carbohydrates and start to store fat. If you want a reminder of what I looked like on an “athlete’s diet” of complex carbs and little saturated fat, coupled with 3 to 4 hours of exercise a day, look here, here, and here. On the other hand, my wife can eat a bag of Oreo cookies for dinner every night, coupled with all the pasta, bread, and rice the world has to offer and not put on one pound (she has weighed about 110 pounds her entire adult life). How is this possible? Does this mean insulin doesn’t control fat metabolism? No, it means we have an entirely different genetic make-up. Her grandmother is 86 years old, eats bread all day long, is healthy as a horse, and weighs 100 pounds. Conversely, I come from a family where every single man has died of heart disease and looked like the Pillsbury Dough Boy prior to doing so. I’m genetically programmed to lean towards metabolic syndrome, but I’ve been able to reverse it through strict attention to my eating habits.
This isn’t unique to me and my wife. There is an entire spectrum – a distribution across the population – of people with varying degrees of susceptibilities to the effects of carbohydrate on insulin levels and the commensurate effects of insulin levels on fat storage and breakdown.
And like gravity, the effect of insulin on our metabolism of fat changes over time at the individual level, usually for the worse.
Consider, again, my example: When I was 16 years old I weighed 160 pounds, had between 4 and 5% body fat, a 28-inch waist and a 44-inch chest. Breakfast consisted of a box (not a bowl) of cereal. Lunch consisted of 7 turkey and tuna sandwiches (yes, 14 pieces of bread), a gallon of apple juice, and a plate of fries and gravy. Dinner was a pound of pasta and half a chicken. Despite eating over 1,000 gm of carbohydrate per day, I was quite resistant to them (i.e., I was very insulin sensitive) and remained exceptionally lean.
Fast forward to three years ago, at the age of 36, I weighed 200 pounds, had 25% body fat, a 36-inch waist and a 44-inch chest. What changed over 20 years? I was actually eating considerably less – in both absolute amounts and total carbohydrates – and yes, I was exercising a bit less (3 to 4 hours per day at 36 versus 6 hours per day when I was 16). But, is that the only thing that changed? What changed in me, and what changes in most people over the same period of their lives, is that I became progressively more insulin resistant. Most people casually observe that their “metabolism slows down” as they age, but what really happens?
I wish I could definitively tell you why this happens. I can’t. What I can tell you is how it happens. There are many factors, and they certainly vary by person and by individual significance. The list below is a bit simplified and by no means complete.
Over time, endogenous production of sex hormones (e.g., testosterone, estrogen) becomes altered, and this seems to play a role in fat metabolism. In addition to sex hormones, other non-sex steroid hormones (e.g., cortisol), which have a strong effect on fat metabolism, may be altered for a variety of reasons including sleep reduction and stress.
Perhaps (at least partially) related to this, the cellular distribution and density of lipoprotein lipase (LPL) also changes. [Recall, LPL is a very important enzyme on the surface of muscle cells and fat cells. On muscle cells, it fosters fat oxidation (good). On fat cells, it fosters fat accumulation (bad).] As we age, we tend to have less LPL on muscle cells and more LPL on fat cells, both of which contribution to fat accumulation rather than fat oxidation.
The membranes of our cells tend to change in fatty acid composition, which may result in more difficulty getting the GLUT-4 transporter into cell membranes to foster glucose flux into cells. I describe this process in this video. The more difficult it is to get glucose into cells, the more insulin the pancreas must secrete to exert its eventual effect, the more exposure all cells have to circulating insulin levels. Higher levels of insulin also exacerbate the phenomenon of more LPL on fat cells and reduced fat oxidation.
These changes are all linked, and probably play a different role of importance in different people at different times in our lives.
What this means effectively is that a 2,500-calories-a-day high-protein diet adds fewer calories to the body than a 2,500-calories-a-day high-carb diet, which in turn adds fewer calories to the body than a 2,500-calories-a-day high-fat diet.
a Japanese study found that boxers placed on a six-meals-a-day weight-control diet lowered their body fat percentage significantly more than boxers who ate exactly the same number of calories in just two meals.
miffy49 wrote: Barry Groves formula is 10 to 15% of cals as carb, 20 to 30% as protein and 60 to 70% as fat. That seems on the low side compared to some of the LCHF disciples. Most go for at least 75% of cals as fat. I don't have any links but hopefully Caro will.
Once you get over 70% I find it all gets a bit unpleasant. I did once try the Atkins Fat Fast which is 90% fat. To be fair they do suggest only 3-5days at that level but its not the sort of diet I would want to live with!
do you know what the cause was?
CreakyPete wrote: Rawkaren - if you mean Atkins, he died at 72 from a heart problem that was not apparently related to blocked arteries. See Wikipedia; there were attempts by anti-atkins journalists etc to discredit his diet on the basis of his weight at the time of death but he put on loads during his time in hospital, supposedly water retention.
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