Hopefully, that got your attention! Please watch the following video.
The video is about teaching youngsters to develop the critical thinking skills necessary to make healthy food choices.
The secret to successful weight loss & maintenance:-
Formulate a good plan. A good plan is one that works and is sustainable. Exercise mainly increases fitness, but also increases energy expenditure. See Calories Burned - Walking: 3.5 mph (17 minutes per mile). E.g. a 250lb man who walks for 45 minutes expends 378kcals.
The vast majority of people who visit "fast food" establishments don't have the critical thinking skills necessary to make healthy food choices. "Fast food" establishments use every marketing trick in the book to influence people to make unhealthy food choices and consume as much of them as possible.
As people are reluctant to go back for second helpings (as they think it makes them look greedy), super-sizing was invented, which allows people to eat considerably more food for not much extra money.
Delicious aromas increase hedonic hunger. Added sugar, salt and flavour enhancers make foods moreish.
Bright colours, cartoon characters and toys attract children.
Edward Bernays-style (emotion-targeted) marketing encourages people to visit "Fast food" establishments, make unhealthy food choices and over-consume them. See https://www.dailymotion.com/video/x2d29tf for more information. The first two minutes summarise.
Showing posts with label Hypocaloric diets. Show all posts
Showing posts with label Hypocaloric diets. Show all posts
Tuesday, 20 October 2015
Friday, 26 April 2013
The most simple tip to lose weight EVER is “Eat less and move more”.
Said Gaz at Cycle Of Life - Fix You.
He went from this...
To this...
Now tell me that ELMM doesn't work!
He went from this...
 |
| Not a happy bunny. |
 |
| A happy bunny. |
Monday, 25 June 2012
Adipocyte Hyperplasia - Good or Bad?
The answer is "It depends!".
The above plot is from Fig. 4 of 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 and shows that leptin secretion from adipocytes increases non-linearly with increasing culture period.
As adipocytes fill, there's insignificant leptin secretion up to a certain level of fullness. Above that level of fullness, leptin secretion increases non-linearly. What this means is that reducing adipocyte fullness by x% reduces leptin secretion by more than x%.
If adipocytes become full due to a chronic caloric excess, there are four permutations of continued caloric excess/subsequent caloric deficit & hyperplasia/no hyperplasia.
1a: There is continued caloric excess. No preadipocytes are converted into adipocytes i.e. there is no adipocyte hyperplasia. There is no additional storage capacity available for excess nutrients, so they remain in circulation. T2DM has developed = bad.
1b: There is subsequent caloric deficit, adipocytes start to deplete, storage capacity becomes available and T2DM goes away (if beta cells haven't been destroyed). The low number of fairly full adipocytes secrete sufficient leptin, so metabolic rate is high and hunger is low = good.
2a: There is continued caloric excess. Pre-adipocytes are converted into adipocytes i.e. there is adipocyte hyperplasia. There is additional storage capacity available for excess nutrients, so T2DM doesn't develop = good.
2b: There is subsequent caloric deficit. Adipocytes start to deplete. However, there are more adipocytes than in 1b, so for a given fat mass, adipocytes are less full than in 1b. The higher number of less full adipocytes secrete less leptin than in 1b, so metabolic rate is lower and hunger is higher than in 1b = bad.
Adipocyte hyperplasia is good for preventing T2DM as fat mass increases, but bad for metabolic rate and hunger after subsequent fat mass loss. Children are growing, so have adipocyte hyperplasia. Adults aren't growing, so have less/no adipocyte hyperplasia. Therefore, adipocyte hyperplasia during childhood will result in some protection from developing T2DM, but life-long misery due to increased hunger and reduced metabolic rate after subsequent fat mass loss. This is why I believe that children need to be protected from the persuasive marketing of manufacturers of CIAB (Crap-in-a-Bag/Box/Bottle).
See Beradinelli-Seip Syndrome – stick that in your pipe and smoke it and read the comments to see why adults with insufficient adipocytes are highly likely to develop T2DM. This is why Asians who remain skinny in childhood (so have no adipocyte hyperplasia) have a high risk of developing T2DM. Sumo wrestlers are Asians who become fat in childhood (so they have a lot of adipocyte hyperplasia) so they have a lower risk of developing T2DM.
According to 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."
If you want to remain slim, high fasting serum insulin due to hepatic and/or muscular insulin resistance and/or chronic overconsumption is bad.
The above plot is from Fig. 4 of 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 and shows that leptin secretion from adipocytes increases non-linearly with increasing culture period.
As adipocytes fill, there's insignificant leptin secretion up to a certain level of fullness. Above that level of fullness, leptin secretion increases non-linearly. What this means is that reducing adipocyte fullness by x% reduces leptin secretion by more than x%.
If adipocytes become full due to a chronic caloric excess, there are four permutations of continued caloric excess/subsequent caloric deficit & hyperplasia/no hyperplasia.
1a: There is continued caloric excess. No preadipocytes are converted into adipocytes i.e. there is no adipocyte hyperplasia. There is no additional storage capacity available for excess nutrients, so they remain in circulation. T2DM has developed = bad.
1b: There is subsequent caloric deficit, adipocytes start to deplete, storage capacity becomes available and T2DM goes away (if beta cells haven't been destroyed). The low number of fairly full adipocytes secrete sufficient leptin, so metabolic rate is high and hunger is low = good.
2a: There is continued caloric excess. Pre-adipocytes are converted into adipocytes i.e. there is adipocyte hyperplasia. There is additional storage capacity available for excess nutrients, so T2DM doesn't develop = good.
2b: There is subsequent caloric deficit. Adipocytes start to deplete. However, there are more adipocytes than in 1b, so for a given fat mass, adipocytes are less full than in 1b. The higher number of less full adipocytes secrete less leptin than in 1b, so metabolic rate is lower and hunger is higher than in 1b = bad.
Adipocyte hyperplasia is good for preventing T2DM as fat mass increases, but bad for metabolic rate and hunger after subsequent fat mass loss. Children are growing, so have adipocyte hyperplasia. Adults aren't growing, so have less/no adipocyte hyperplasia. Therefore, adipocyte hyperplasia during childhood will result in some protection from developing T2DM, but life-long misery due to increased hunger and reduced metabolic rate after subsequent fat mass loss. This is why I believe that children need to be protected from the persuasive marketing of manufacturers of CIAB (Crap-in-a-Bag/Box/Bottle).
See Beradinelli-Seip Syndrome – stick that in your pipe and smoke it and read the comments to see why adults with insufficient adipocytes are highly likely to develop T2DM. This is why Asians who remain skinny in childhood (so have no adipocyte hyperplasia) have a high risk of developing T2DM. Sumo wrestlers are Asians who become fat in childhood (so they have a lot of adipocyte hyperplasia) so they have a lower risk of developing T2DM.
According to 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."
If you want to remain slim, high fasting serum insulin due to hepatic and/or muscular insulin resistance and/or chronic overconsumption is bad.
Sunday, 4 January 2009
Everybody knows.........Part 1
Yesterday, on a message-board 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."
"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."
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