Since I’m in the middle of writing a book for kids, articles about kids and health that land in my inbox receive special attention. Two recent articles illustrate what’s wrong with the prevailing advice on how to reduce rates of childhood obesity.
That advice, of course, is to cajole, harass, or possibly shame kids into eating less and exercising more. (Strangely, there were few fat kids in my grade school despite a lack of cajoling and harassing.) The USDA-approved lunches are lower in fat and calories than in previous years, and we’ve got federal campaigns like Let’s Move! to promote exercise.
Again, nobody had to cajole kids into moving when I was growing up. Playing outside with friends is what we lived for. If anything, our moms had to yell out the back door and demand we stop playing and come inside for dinner. I’m pretty sure once kids reach the point where they don’t naturally want to move, cajoling won’t make much of a difference.
A recent study supports that point. Here are some quotes from a Science Daily article titled Guilting teens into exercise won’t increase activity:
Just like attempts at influencing hairstyles or clothing can backfire, adults who try to guilt middle-schoolers into exercising won’t get them to be any more active, according to a new study by University of Georgia researchers.
The study, which appears in the September issue of the journal Medicine & Science in Sports & Exercise, found students who don’t feel in control of their exercise choices or who feel pressured by adults to be more active typically aren’t. Middle-schoolers who feel they can make their own decisions about exercising are more likely to see themselves as a person who exercises, which in turn makes them more likely to exercise.
Hmmm … it would be easy to read that and conclude that if you put pressure on kids, they don’t want to exercise, but if you don’t put pressure on them, they do want to exercise. Defiant little tykes, eh?
I think the more likely explanation is that kids who don’t enjoy being active end up being pressured to exercise (because people think they’re lazy), while kids who naturally want to move aren’t pressured. So the associations show up as pressured = less active, not pressured = active.
This age is a critical juncture in a child’s life, as kids typically decrease their activity levels by 50 percent between fifth and sixth grades, said Rod Dishman, the study’s lead author and a professor of kinesiology in the UGA College of Education.
“Our results confirm that the beliefs these kids hold are related to physical activity levels,” Dishman said. “But can we put these children in situations where they come to value and enjoy the act of being physically active?”
Dishman and colleagues at the University of South Carolina are now looking at ways to help kids identify with exercise at a younger age, so that by the time they reach middle school they are more likely to identify as someone who exercises.
I seriously doubt kids exercise because they identify themselves as someone who exercises. I think it’s likely the other way around: they identify themselves as someone who exercises because they enjoy being active. I identify myself as a disc golfer because I enjoy the game, so I play it. I didn’t take up disc golf because I identified myself as a disc golfer.
What parents and teachers don’t want to create, Dishman cautioned, is a sense of guilt for not exercising. The research overwhelmingly found that students who felt obligated to be more active were less likely to embrace activity overall.
“The best thing is to do it because it’s fun,” Dishman said. “It’s the kids who say they are intrinsically motivated who are more active than the kids who aren’t.”
BINGO. The kids who are intrinsically motivated are feeling what Gary Taubes calls the compulsion to move. Their bodies would rather burn calories than store them, so they feel full of energy. They want to be active.
The kids whose bodies are in calorie-storage mode, on the other hand, don’t feel like moving. They don’t have the energy. Exercise feels like a chore. The research is clear on the chicken-or-the-egg question: kids don’t get fat because they stop moving. They start getting fat first, then stop moving.
That means the problem is diet, which brings us to the other interesting article to land in my inbox. Here are some quotes from an article published by the University of Missouri School of Medicine:
Although health experts recommend breakfast as a strategy to reduce an individual’s chance of obesity, little research has examined if the actual type of breakfast consumed plays a significant role in one’s health and weight management.
Of course the type of breakfast plays a significant role. Does anyone think Pop-Tarts and eggs produce the same hormonal effects?
University of Missouri researchers compared the benefits of consuming a normal-protein breakfast to a high-protein breakfast and found the high-protein breakfast — which contained 35 grams of protein — prevented gains of body fat, reduced daily food intake and feelings of hunger, and stabilized glucose levels among overweight teens who would normally skip breakfast.
Heather Leidy, PhD, an assistant professor in the Department of Nutrition and Exercise Physiology at the MU School of Medicine and lead author of the study, said the key to eating 35 grams of protein is to consume a combination of high-quality proteins including milk, eggs, lean meats and Greek yogurt.
I don’t think the meat necessarily has to be lean, but a big YES on the protein. Protein intake has a strong effect on appetite.
Leidy and her colleagues fed two groups of overweight teens ,who reported skipping breakfast between five and seven times a week, either normal-protein breakfast meals or high-protein breakfast meals. A third group of teens continued to skip breakfast for 12 weeks.
“The group of teens who ate high-protein breakfasts reduced their daily food intake by 400 calories and lost body fat mass, while the groups who ate normal-protein breakfast or continued to skip breakfast gained additional body fat,” Leidy said. “These results show that when individuals eat a high-protein breakfast, they voluntarily consume less food the rest of the day. In addition, teens who ate high-protein breakfast had more stable glucose levels than the other groups.”
Give kids more protein, and they spontaneously eat less. No cajoling or harassing required. They eat less because they’re not as hungry, period. Same goes for adults, by the way. That shows up in the research over and over.
So let’s take a look at what the geniuses behind the Healthy, Hunger-Free Kids Act (championed by The First Lady, as the USDA site informs us right at the top) require for federally-approved school breakfasts.
A cup of fruit per day is required. Grains are required. A cup of milk is required, but of course that would be skim milk – although it can be “flavored,” according to a different document. That means chocolate or strawberry milk with sugar. There’s no meat or even a meat alternative required – although in the footnotes, you can find this gem:
Beginning July 1, 2013 (SY 2013-2014), schools may substitute 1 oz. eq. of meat/meat alternate for 1 oz. eq. of grains after the minimum daily grains requirement is met.
Well, that is just damned generous of the feds to allow schools to swap an ounce of meat for an ounce of grains … after the minimum daily grains requirement is met. Kids just can’t be healthy without those grains, ya know.
So according to the USDA, this is the breakfast that will give us healthy, hunger-free kids: fruit, grains, and fat-free milk with sugar. No meat or eggs required.
And that’s why people think kids need to be pressured into eating less and moving more: they’re put on diets that make them want to eat more and move less. Then people blame the kids.
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Take statins to protect your heart and you’ll live a long time!
No, wait … you’ll just feel like you’ve been living a long time.
Here are some quotes from an article in the UK Express titled Statins: Heart disease drug speeds up ageing process, warns new research.
Statins make regular users become older faster, leaving them open to long-term mental and physical decline, according to disturbing new research.
Scientists have found the heart disease drug badly affects our stem cells, the internal medical system which repairs damage to our bodies and protects us from muscle and joint pain as well as memory loss.
You mean artificially beating down your cholesterol — one of the primary structural components of your brain — can affect your memory? I’d forgotten that. No, wait … I didn’t forget that. Good thing I don’t take statins.
Last night experts warned patients to “think very carefully” before taking statins as a preventative medicine.
And if they’re not on statins yet, they may actually be able to think very carefully.
The new research by scientists at Tulane University in New Orleans has reignited the debate about statin side effects which many doctors say have been played down.
Those are the good doctors. The bad doctors help play down the side effects, often by ignoring them or attributing them to old age. Hey, wait a minute … maybe that aging thing is fooling the doctors.
“Doctor, I think this statin might not be so good for me. I ache all the time, I’m tired, and I’m getting forgetful.”
“Well, that’s not unusual for an 80-year-old man.”
“I’m 62, Doctor.”
“Oh. Well, you seem 80 to me, so my point stands.”
Professor Reza Izadpanah, a stem cell biologist and lead author of the research published in the American Journal of Physiology, said: “Our study shows statins may speed up the ageing process.
“People who use statins as a preventative medicine for health should think again as our research shows they may have general unwanted effects on the body which could include muscle pain, nerve problems and joint problems.”
The scientists who treated stem cells with statins under laboratory conditions found that after a few weeks the cholesterol-busting treatment had a dramatic effect.
Statins prevented stem cells from performing their main functions, to reproduce and replicate other cells in the body to carry out repairs. The researchers found the statins prevented stem cells from generating new bone and cartilage.
Wow, awesome drug. When the patents finally run out, maybe the manufacturers can drop the price and sell high doses of the stuff as rat poison.
Dr Malcolm Kendrick, a GP in Macclesfield, Cheshire, who has studied heart health and statins, said: “Statins just make many patients feel years older. This research reinforces what has long been suspected. The side effects of statins mimic the ageing process.
“I observe patients on statins slowing down. Some are not affected, for some it is a relatively subtle process, but for many it is a serious side effect and one which disturbingly helps us confirm what we have long suspected.”
Kendrick is so honest about the state of modern medicine, I’m surprised he still has a medical license.
Professor Izadpanah said: “People at high risk of heart disease can reduce this risk by taking statins. However, considering the adverse effects of these drugs and their association with so many side effects, it is crucial people are fully aware of the risks before they take the treatment.”
Making people fully aware of the risks isn’t in the interest of the statin-makers or the doctors who prescribe them. That’s why you and I have to keep shouting this stuff from the hilltops.
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One of the managers at work has another project in mind he’d like me to take on. Since I’m already working on a big project, he wondered aloud in a meeting if I’d consider cloning myself.
Heck, if I could clone myself, I would have already done it. It’s almost October, and I still have miles to go on that book project — which I originally wanted to have written last October. Programming job, blogging, book writing, weekend farm chores, a bit of R & R time with Chareva and the girls … there just aren’t enough hours in a week.
So for now, I’m going to reduce the blogging workload to one post per week on Thursday. My Monday-evening writing sessions will be dedicated to the book instead of the blog.
Promise I’ll do my best to make the book worth the wait.
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A dietary shift is definitely happening. Here’s how I know that for sure:
The big-money bankers are on board.
In case you didn’t see it in the comments section of my most recent post, Credit Suisse just published an 84-page report titled Fat: The New Health Paradigm. I skimmed it and was impressed, but my initial response was why is a bank publishing this?
The answer (echoed by a handful of readers) is that Credit Suisse is an investment bank, and their reports are intended to inform investors of economic trends. If there’s a big movement among consumers to embrace natural fats and cut back on grains and vegetable oils, that will of course have an economic impact. Probably not a good time to invest in General Mills.
Two of the bullet points from the document’s summary section make that clear:
- What is the outlook? Globally, we expect fat to grow from the current 26% of calorie intake to 31% by 2030, with saturated fat growing the fastest and going from 9.4% of total energy intake to 13%. This implies that fat consump¬tion per capita will grow 1.3% a year over the next fifteen years versus a rate of 0.9% over the last fifty years. We expect saturated fat to grow at 2% a year versus a historical rate of 0.6% a year; monounsaturated at 1.3% a year versus 1.0%; polyunsaturated omega-6 to decline 0.2% a year versus a 1.3% past growth rate and polyunsaturated omega-3 to grow at 0.7% a year versus 1.6% a year over the last 50 years.
- Among foods, the main winners are likely to be eggs, milk and dairy products (cheese, yogurt and butter) and nuts with annual rates of growth around 2.5-4%. The losers are likely to be wheat and maize and to a lesser extent solvent-extracted vegetable oils. Meat consumption per capita should grow at 1.4% a year and fish at 1.6% supported by a fast expanding aquacul¬ture industry.
But there’s waaaaay more to the report than predictions of what consumers will be buying or not buying in the near future. There are explanations of the various types of fats, a history of fat in the human diet, and a history of the anti-fat hysteria that took hold in the 1960s and became official policy in the 1980s. There’s a lovely, concise section that looks at the evidence (more like lack of evidence) that fat causes heart disease and obesity. There’s a similar section on the health effects of red meat. And of course, there are sections on the recent shift in consumer attitudes about fat.
I’m still reading the thing (since I have a full-time job and all that), but here’s a sample of other bullet points from the opening summary:
- Triangulating several topics such as anthropology, breast feeding, evolution of primates, height trends in the human population, or energy needs of our various vital organs, we have concluded that natural fat consumption is lower than “ideal” and if anything could increase safely well beyond current levels.
- The 1960s brought a major change in the perception of fat in the world and particularly in the U.S., where saturated fat was blamed for being the main cause behind an epidemic of heart attacks. We will see that it was not saturated fat that caused the epidemic as its consumption declined between 1930 and 1960. Smoking and alcohol were far more likely factors behind the heart attack epidemic.
- Saturated fat has not been a driver of obesity: fat does not make you fat. At current levels of consumption the most likely culprit behind growing obesity level of the world population is carbohydrates. A second potential factor is solvent-extracted vegetable oils (canola, corn oil, soybean oil, sunflower oil, cottonseed oil). Globally consumption per capita of these oils increased by 214% between 1961 and 2011 and 169% in the U.S. Increased calories intake—if we use the U.S. as an example—played a role, but please note that carbohydrates and vegetable oils accounted for over 90% of the increase in calorie intake in this period.
- A proper review of the so called “fat paradoxes” (France, Israel and Japan) suggests that saturated fats are actually healthy and omega-6 fats, at current levels of consumption in the developed world, are not necessarily so.
- Doctors and patients’ focus on “bad” and “good” cholesterol is superficial at best and most likely misleading. The most mentioned factors that doctors use to assess the risk of CVDs—total blood cholesterol (TC) and LDL cholesterol (the “bad” cholesterol)—are poor indicators of CVD risk. In women in particular, TC has zero predictive value if we look at all causes of death. Low blood cholesterol in men could be as bad as very high cholesterol. The best indicators are the size of LDL particles (pattern A or B) and the ratio of TG (triglycerides) to HDL (the “good” cholesterol). A VAP test to check your pattern A/B costs less than $100 in the U.S., yet few know of its existence.
- Based on medical and our own research we can conclude that the intake of saturated fat (butter, palm and coconut oil and lard) poses no risk to our health and particularly to the heart. In the words of probably the most important epidemiological study published on the subject by Siri-Tarino et al: “There is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.” Saturated fat is actually a healthy source of energy and it has a positive effect on the pat¬tern A/B.
- The main factor behind a high level of saturated fats in our blood is actually carbohydrates, not the amount of saturated fat we eat.
Wow. Great stuff … from a bank.
In case you had any doubts that most doctors don’t keep up with the latest diet and health research, the report includes this finding:
We conducted two proprietary surveys of doctors, nutritionist and consumers to understand better their perception of the issues we mentioned previously. All three groups showed superficial knowledge on the potential benefits or risks of increased fat consumption. Their views are influenced significantly more by public health bodies or by WHO and AHA rather than by medical research. Even on the “easy” topic of cholesterol, 40% of nutritionists and 70% of the general practitioners we surveyed still believe that eating cholesterol-rich foods is bad for your heart.
Go figure. The nutritionists are more likely than doctors to know that cholesterol has been found not guilty of causing heart disease.
In term of macronutrients, 45% of the doctors surveyed said that their perception of protein has improved, versus only 5% saying it has worsened; 29% of the doctors said that their perception of fat has improved versus only 7% saying it has worsened; and 15% only said that their perception of carbohydrates has improved versus 26% saying it has worsened.
Answering what makes you fat if eaten in large quantities, the doctors correctly pointed to sugar and carbohydrates (32% and 26%); fat and saturated fats are not as bad (23% and 16%) and protein collected only 2% of the responses.
However, the doctors believed that the best diet for weight loss is a low calorie one (65%), followed by low carbohydrate (36%) and low fat (7%). Among nutritionists, 42% prefer the low carbohydrate diet, against 30% for the general practice group.
Let’s focus on the positive. Yes, nearly two-thirds of doctors surveyed believe low-calorie diets are best for weight loss, but only 7% recommended a low-fat diet, versus 36% who recommended a low-carb diet. I’d wager a large sum that 15 or 20 years ago, more doctors would have been recommending a low-fat diet than a low-carb diet. It’s progress. And I was pleasantly surprised to see that 42% of the nutritionists recommend a low-carb diet.
I plan to read the entire report when I can. If anything jumps out at me as particularly interesting, I’ll post about it.
In the meantime, I see this report as another sign that the arterycloggingsaturatedfat! paradigm is dying out. The American Heart Association doesn’t want it to happen, The Guy From CSPI doesn’t want it to happen, the USDA Dietary Guidelines Committee doesn’t want it to happen, and countless makers of low-fat and low-cholesterol food-like products don’t want it to happen. But it’s happening.
And you can take that to the bank.
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My previous post quoted from a study in which researchers induced rats to overeat and gain weight by injecting them with insulin – a.k.a. the “acute appetite suppressant,” according to some.
I’m not usually a big fan of rat studies because of how they’re conducted. Researchers will feed fats a high-fat (ahem) “Atkins” diet of frankenfats, casein and corn starch, then pretend the results have some bearing on how a diet of meats and eggs will affect the health of human beings. The study I cited in my last post, however, wasn’t a diet study. It was study of how a hormone affects appetite and weight. The insulin was injected directly.
Based on links in the comments, I looked for and found a handful of studies that demonstrate what insulin does to human subjects. Let’s take a look.
In this study, diabetes patients were treated either with 1-2 injections of insulin per day (called the conventional therapy by the researchers) or multiple daily injections (called intensive therapy by the researchers). Here are the results:
Intensively treated patients gained an average of 4.75 kg more than their conventionally treated counterparts (P < 0.0001). This represented excess increases in BMI of 1.5 kg/m(2) among men and 1.8 kg/m(2) among women. Growth-curve analysis showed that weight gain was most rapid during the first year of therapy. Intensive therapy patients were also more likely to become overweight (BMI >or=27.8 kg/m(2) for men, >or=27.3 kg/m(2) for women) or experience major weight gain (BMI increased >or=5 kg/m(2)). Waist-to-hip ratios, however, did not differ between treatment groups. Major weight gain was associated with higher percentages of body fat and greater fat-free mass, but among patients without major weight gain, those receiving intensive therapy had greater fat-free mass with no difference in adiposity.
So people treated more aggressively with insulin ended up gaining about 10 pounds more than those treated with less insulin. For many, the difference was more body fat. For others, it was a mix of more body fat and more lean mass. Well, no surprise there. Insulin spurs growth. That’s some why body-builders shoot the stuff. But if you have a tendency to get fat, higher insulin will make you fatter.
In this study, researchers treated diabetics with a sulphonylurea (drug that stimulates insulin internally), or with insulin directly, or with diet (which was labeled conventional therapy). The goal was to improve glucose control, not weight. But weight changes were included in the results:
Weight gain was significantly higher in the intensive group (mean 2.9 kg) than in the conventional group (p<0.001), and patients assigned insulin had a greater gain in weight (4.0 kg) than those assigned chlorpropamide (2.6 kg) or glibenclamide (1.7 kg).
Subjects who were either stimulated to produce more insulin or given insulin directly gained more weight than those treated with diet, and those given insulin directly gained the most.
In this study, researchers added three different insulin therapies to metformin:
In an open-label, controlled, multicenter trial, we randomly assigned 708 patients with a suboptimal glycated hemoglobin level (7.0 to 10.0%) who were receiving maximally tolerated doses of metformin and sulfonylurea to receive biphasic insulin aspart twice daily, prandial insulin aspart three times daily, or basal insulin detemir once daily (twice if required). Outcome measures at 1 year were the mean glycated hemoglobin level, the proportion of patients with a glycated hemoglobin level of 6.5% or less, the rate of hypoglycemia, and weight gain.
And the conclusion based on the results:
A single analogue-insulin formulation added to metformin and sulfonylurea resulted in a glycated hemoglobin level of 6.5% or less in a minority of patients at 1 year. The addition of biphasic or prandial insulin aspart reduced levels more than the addition of basal insulin detemir but was associated with greater risks of hypoglycemia and weight gain.
More insulin resulted in lower glycated hemoglobin (a.k.a, what’s measured in an A1C test as an indicator of average glucose levels over time), but also in more weight gain.
In this study, researchers put 50 subjects on a weight-loss diet after running a series of lab tests. They wanted to identify which factors predicted success or failure in losing weight and keeping it off. Here’s what they found:
On the basis of body weight trajectories, 3 subject clusters were identified. Clusters A and B lost more weight during energy restriction. During the stabilization phase, cluster A continued to lose weight, whereas cluster B remained stable. Cluster C lost less and rapidly regained weight during the stabilization period. At baseline, cluster C had the highest plasma insulin, interleukin (IL)-6, adipose tissue inflammation (HAM56+ cells), and Lactobacillus/Leuconostoc/Pediococcus numbers in fecal samples. Weight regain after energy restriction correlated positively with insulin resistance (homeostasis model assessment of insulin resistance: r = 0.5, P = 0.0002) and inflammatory markers (IL-6; r = 0.43, P = 0.002) at baseline.
The resistance to weight loss and proneness to weight regain could be predicted by the combination of high plasma insulin and inflammatory markers before dietary intervention.
Yes, there was more going on here than insulin levels – inflammation and a difference in gut bacteria. But the point is that those with high plasma insulin (the “acute appetite suppressant”) lost less weight and regained it more quickly. I don’t think their appetites were suppressed very effectively.
In this study, diabetics were treated with an “intensive program” of insulin for six months. Once again, the goal was glucose control, not weight control. But weight did change:
During treatment, mean serum insulin levels increased from 308 ± 80 to 510 ± 102 pM, while body weight increased from 93.5 ± 5.8 to 102.2 ± 6.8 kg.
After six months, the “intensive program” of insulin led to an average weight gain of just over 19 pounds.
I suppose the explanation from the “insulin is an acute appetite suppressant” crowd would be that these studies were conducted on diabetics who are by definition insulin resistant. Right. And so are a helluva lot of people out there who are overweight and looking for a way to drop the pounds. We see it over and over in these studies: higher insulin, whether produced internally or given as a treatment, leads to more weight gain. Dr. Lustig apparently speaks the truth when he says I can make anyone fat with enough insulin.
(Lustig is an endocrinologist, in case you’ve forgotten. Hormones are his specialty.)
So for the people most desperate to lose weight, the “insulin is an acute appetite suppressant” notion is clearly a load of bologna. If their appetites were acutely suppressed, they wouldn’t be obese; they’d be anorexic. As part of their weight-loss strategy, need to bring down their insulin levels. Period.
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Many of you may recall a kerfuffle raised by a controversial article claiming that we’ve got it all wrong about insulin. Far from being a driver of weight gain, according to the article, insulin is actually an acute appetite suppressant. It makes us less hungry, by gosh, not more.
That article seems to show up on diet-related social media sites on a regular basis. A few weeks ago, some born-to-be-lean jock who joined the Fat Head Facebook group for the sole purpose of being an annoying jackass posted a link to it. I responded, which started a back-and-forth debate.
If insulin is such a fabulous appetite suppressant, I asked, then explain this: type 2 diabetics produce high levels of insulin. They’re also far more likely than other people to be overweight or obese. So why isn’t the acute appetite suppressant causing them to eat less and lose weight?
The response (I’m paraphrasing here): Well, ya see, ya big dummy, type 2 diabetics are insulin resistant by definition. So they don’t experience the effects of the acute appetite suppressant.
Hmmm. Okay, then, explain this one: People will start eating foods that provoke a high insulin response — a big tub of popcorn, or a big bag of chips — swearing to high heaven they’re only going to eat, say, half. Then they eat the whole thing. Then after cursing at themselves for not having any discipline, they go get more. Why isn’t the acute appetite suppressant kicking in and stopping them from eating way more than they intended?
The response (I’m paraphrasing again here): Well, ya see, ya big dummy, the food-reward properties of the popcorn or chips override the appetite-suppressant effect of the insulin.
Ahh, I see. So there’s really no need to adopt a diet that reduces your insulin levels, because insulin is actually an acute appetite suppressant … unless 1) you’re insulin resistant (like so many obese people), or 2) when you reach for high-carb foods, you choose the ones that taste good.
Well, that is fabulous news indeed for all the obese people out there who aren’t insulin resistant and prefer carbohydrate foods with little or no flavor.
I chose not to engage in an endless online debate because I had more important things to do, like write software code for work, take the girls to their piano lessons, and rearrange my shoes by size, color and length of service.
But while digging up some research for the book project, I stumbled across a study abstract that caught my attention because it mentioned something about using insulin to induce weight gain. So I called upon one of my super-secret, deeply embedded, password-protected double-agents in academia to get a copy of the full paper.
The paper, published in 1966, is titled WEIGHT REGULATION IN NORMAL AND HYPOTHALAMIC HYPERPHAGIC RATS.
It’s the normal rats I’m interested in. Here are some quotes from the paper:
To induce overeating and weight gain in normal rats without brain damage, we used periodic injections of long acting insulin. Measurements of body weight and ad-lib food (powdered Purina chow) and water intake were taken on 23 Sherman female rats, housed at 80 ± 2° F. during a 2-wk. control period, 2 wk. of insulin treatment, and a 2-wk. recovery period. The insulin dose was 8 units per injection for the first 3 days, then 12 units thereafter.
Boy, those researchers must have been disappointed. Here they were, hoping to induce overeating and weight gain, and yet they injected the rats with an acute appetite suppressant. Big mistake, obviously.
All rats given protamine zinc insulin increased their food intake, presumably in response to hypoglycemia. In the short term experiment, 11 of the 23 rats survived by consuming nearly twice their normal daily food intake.
The rats who didn’t survive apparently died because they couldn’t eat enough to keep their little bodies fueled while the insulin drove down their blood sugar and locked up their fat cells. They were eating like crazy, but starving at the cellular level.
That reminds me of the conclusion from another paper in my files: appetite is largely a function of how much fuel is available at the cellular level, not how much fuel is consumed.
Their average weight gain was 58 gm. during the 2 wk. of insulin treatment, as compared to 13 gm. during the previous 2 wk.
This confirms the original observations of Mackay et al. (1940) and extends their results to indicate that marked obesity as well as overeating can be produced with insulin.
So marked obesity and overeating can be produced with injections of the acute appetite suppressant. Got it. Well, perhaps the rats injected with insulin just happened to find that powdered Purina chow waaaay more rewarding all of a sudden. Maybe the researchers added salt.
Every rat taken off the insulin regime after 2 wk. ate subnormal amounts of food and lost weight precipitously. On the average they were anorectic for 4 days, and lost 46 gm., which was 79% of the weight previously gained under the influence of insulin.
Researchers stopped injecting the rats with the acute appetite suppressant, and the rats responded by eating less and losing weight.
Boy, that almost sounds like what happened when I jettisoned a lot of insulin-producing foods from my diet. Reduce circulating levels of that acute appetite suppressant, and I’m just not as hungry.
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