Tampilkan postingan dengan label Hypercaloric diets. Tampilkan semua postingan
Tampilkan postingan dengan label Hypercaloric diets. Tampilkan semua postingan

Senin, 25 Juni 2012

Adipocyte Hyperplasia - Good or Bad?

First, a picture. Ignore B, C, D and E.

The above picture is Fig. 4 from Cytokine-mediated modulation of leptin and adiponectin secretion during in vitro adipogenesis: Evidence that tumor necrosis factor-α- and interleukin-1β-treated human preadipocytes are potent leptin producers.

I've posted the above picture to show that leptin secretion increases non-linearly with increasing culture period. As adipocyte content almost certainly increases non-linearly with increasing culture period (like THIS), leptin secretion almost certainly increases very non-linearly with increasing adipocyte content. As adipocyte content increases, there's no/minimal leptin secretion up to a certain level of fullness. Above this level of fullness, leptin secretion increases rapidly. What this means is that reducing adipocyte content by x% reduces leptin secretion by much more than x%.

If somebody's adipocytes become 100% full due to caloric excess, there are two extreme possibilities.

1a: If there is continued caloric excess, no preadipocytes are converted into adipocytes. There is no storage capacity available for excess nutrients, so they remain in circulation. T2DM has developed - BAD.

1b: If there is subsequent caloric deficit, adipocytes start to deplete, storage capacity becomes available and T2DM goes away (if beta cells haven't been completely destroyed in the meantime). The relatively full adipocytes secrete plenty of leptin, so metabolic rate is high and hunger is low - GOOD.

2a: If there is continued caloric excess, pre-adipocytes are converted into adipocytes. This is adipocyte hyperplasia. There is storage capacity available for excess nutrients, so T2DM doesn't develop - GOOD.

2b: If there is subsequent caloric deficit, adipocytes start to deplete. However, there are more adipocytes than in 1), so for a given fat mass, adipocytes are emptier than in 1). The greater number of emptier adipocytes secrete less leptin than in 1), so metabolic rate is lower and hunger is higher than in 1) - BAD.

Adipocyte hyperplasia is good for preventing T2DM as fat mass increases, but bad for metabolic rate and hunger after subsequent fat mass loss. I believe that growing children are much more likely to get adipocyte hyperplasia than adults. Therefore, childhood obesity is highly likely to result in misery after subsequent fat mass loss. This is why I believe that growing children should be protected from the evul greedy manufacturers of Crap-in-a-Bag/Box/Bottle (CIAB).

EDIT: Jane Karlsson just e-mailed me a link to the following study:- Adipocyte Turnover: Relevance to Human Adipose Tissue Morphology.
"Occurrence of hyperplasia (negative morphology value) or hypertrophy (positive morphology value) was independent of sex and body weight but correlated with fasting plasma insulin levels and insulin sensitivity, independent of adipocyte volume (β-coefficient = 0.3, P < 0.0001). Total adipocyte number and morphology were negatively related (r = −0.66); i.e., the total adipocyte number was greatest in pronounced hyperplasia and smallest in pronounced hypertrophy. The absolute number of new adipocytes generated each year was 70% lower (P < 0.001) in hypertrophy than in hyperplasia, and individual values for adipocyte generation and morphology were strongly related (r = 0.7, P < 0.001). The relative death rate (∼10% per year) or mean age of adipocytes (∼10 years) was not correlated with morphology."

So, if you want to remain slim, high fasting serum insulin (due to hepatic and/or muscular insulin resistance) is bad mmm-kay?

Minggu, 04 Januari 2009

Everybody knows.........Part 1

Yesterday, on a messageboard in a galaxy far far away, I was informed by a Nutritionist with letters after her name:-

"As a health and fitness scientist, I have to agree with the overwhelming body of peer reviewed evidence that shows high fat diets are dangerous over a long period of time, and that an athletic diet includes complex carbs taken regularly throughout the day."

To which I replied:-

"Apart from epidemiological evidence (which is highly suspect as there are too many variables), can you show me some solid evidence that "high fat" hypocaloric or isocaloric diets are dangerous over a long period of time? Obviously, high fat hypercaloric diets are dangerous as they cause weight gain.....as do all hypercaloric diets."

Followed by:-

"What if what you were taught was wrong? Read Dr. Schwarzbein's Personal Experiences - Background to first book.

"In medical training, I was taught that a low-fat diet high in complex carbohydrates prevented weight gain and disease. I believed what my professors said. Early on, I advocated low-fat diets. But this soon changed."

Practical experience showed that what she'd been taught was wrong. Just bear that in mind. Obviously, athletes have different dietary requirements to fat people with type 2 diabetes. However, suggesting that all athletes eat "complex carbs" (you shouldn't use the expression "complex carbs" as amylopectin & maltodextrin are complex carbs that turn into blood glucose as quickly as glucose) regularly throughout the day, whether bulking or cutting is wrong.

Cheers, Nige."