Food Reward: a Dominant Factor in Obesity, Part I

A Curious Finding

It all started with one little sentence buried in a paper about obese rats. I was reading about how rats become obese when they're given chocolate Ensure, the "meal replacement drink", when I came across this:

...neither [obesity-prone] nor [obesity-resistant] rats will overeat on either vanilla- or strawberry-flavored Ensure.

The only meaningful difference between chocolate, vanilla and strawberry Ensure is the flavor, yet rats eating the chocolate variety overate, rapidly gained fat and became metabolically ill, while rats eating the other flavors didn't (1). Furthermore, the study suggested that the food's flavor determined, in part, what amount of fatness the rats' bodies "defended."

As I explained in previous posts, the human (and rodent) brain regulates the amount of fat the body carries, in a manner similar to how the brain regulates blood pressure, body temperature, blood oxygenation and blood pH (2). That fact, in addition to several other lines of evidence, suggests that obesity probably results from a change in this regulatory system. I refer to the amount of body fat that the brain defends as the "body fat setpoint", however it's clear that the setpoint is dependent on diet and lifestyle factors. The implication of this paper that I could not escape is that a food's flavor influences body fatness and probably the body fat setpoint.

An Introduction to Food Reward

The brain contains a sophisticated system that assigns a value judgment to everything we experience, integrating a vast amount of information into a one-dimensional rating system that labels things from awesome to terrible. This is the system that decides whether we should seek out a particular experience, or avoid it. For example, if you burn yourself each time you touch the burner on your stove, your brain will label that action as bad and it will discourage you from touching it again. On the other hand, if you feel good every time you're cold and put on a sweater, your brain will encourage that behavior. In the psychology literature, this phenomenon is called "reward," and it's critical to survival.

The brain assigns reward to, and seeks out, experiences that it perceives as positive, and discourages behaviors that it views as threatening. Drugs of abuse plug directly into reward pathways, bypassing the external routes that would typically trigger reward. Although this system has been studied most in the context of drug addiction, it evolved to deal with natural environmental stimuli, not drugs.

As food is one of the most important elements of survival, the brain's reward system is highly attuned to food's rewarding properties. The brain uses input from smell, taste, touch, social cues, and numerous signals from the digestive tract* to assign a reward value to foods. Experiments in rats and humans have outlined some of the qualities of food that are inherently rewarding:

• Fat
• Starch
• Sugar
• Salt
• Meatiness (glutamate)
• The absence of bitterness
  
• Certain textures (e.g., soft or liquid calories, crunchy foods)
• Certain aromas (e.g., esters found in many fruits)
• Calorie density ("heavy" food)
  

We are generally born liking the qualities listed above, and aromas and flavors that are associated with these qualities become rewarding over time. For example, beer tastes terrible the first time you drink it because it's bitter, but after you drink it a few times and your brain catches wind that there are calories and a drug in there, it often begins tasting good. The same applies to many vegetables. Children are generally not fond of vegetables, but if you serve them spinach smothered in butter enough times, they'll learn to like it by the time they're adults.

The human brain evolved to deal with a certain range of rewarding experiences. It didn't evolve to constructively manage strong drugs of abuse such as heroin and crack cocaine, which overstimulate reward pathways, leading to the pathological drug seeking behaviors that characterize addiction. These drugs are "superstimuli" that exceed our reward system's normal operating parameters. Over the next few posts, I'll try to convince you that in a similar manner, industrially processed food, which has been professionally crafted to maximize its rewarding properties, is a superstimulus that exceeds the brain's normal operating parameters, leading to an increase in body fatness and other negative consequences.


* Nerves measure stomach distension. A number of of gut-derived paracrine and endocrine signals, including CCK, PYY, ghrelin, GLP-1 and many others potentially participate in food reward sensing, some by acting directly on the brain via the circulation, and others by signaling indirectly via the vagus nerve. More on this later.

PROBIOTIC REDUCES RECURRENT URINARY TRACT INFECTION

In a randomized, double-blind phase 2 study, an intravaginal probiotic composed of Lactobacillus crispatus CTV-05 (Lactin-V, Osel Inc) reduced the rate of recurrent urinary tract infection (rUTI) in UTI-prone women by roughly one half, which compares favorably with historical data on antimicrobial prophylaxis, the researchers say.
They add that larger trials are warranted to see whether use of vaginal Lactobacillus could replace long-term antimicrobial preventive treatments in women susceptible to rUTI.
The study was published online April 15 and in the May 15 print issue of Clinical Infectious Diseases.
UTIs are common in women and frequently recur, Ann Stapleton, MD, from the University of Washington in Seattle, and colleagues note in their report. It has been shown, they add, that women with rUTIs often have alterations in vaginal microbiota, including depletion of lactobacilli.
A phase 1 study of Lactobacillus crispatus CTV-05 showed that the probiotic can be given as a vaginal suppository with minimal adverse effects to healthy women with a history of rUTI. In the phase 2 study, 100 premenopausal women (median age, 21 years) with a history of rUTI received antimicrobials for acute UTI and then were randomly assigned to receive eitherLactobacillus crispatus CTV-05 or placebo vaginal suppository gelatin capsules administered once daily for 5 days, followed by once weekly for 10 weeks.
"We found that Lactin-V reduced the risk of rUTI approximately as effectively as antimicrobial prophylaxis, achieved high-level vaginal colonization in most women, and was well tolerated," Dr. Stapleton and colleagues report.
According to the investigators, culture-confirmed rUTI occurred in 7 (15%) of 48 of women who received Lactobacillus crispatus CTV-05 compared with 13 (27%) of 48 women who received placebo (relative risk [RR], .5; 95% confidence interval [CI], .2 - 1.2).
A high level of vaginal colonization with L crispatus throughout follow-up was associated with a significant reduction in rUTI only among women receiving Lactobacillus crispatus CTV-05 (RR for Lactin-V, .07; RR for placebo, 1.1; P < .01).
The safety profile of the probiotic mirrored that seen in the phase 1 study. Adverse effects were reported by 56% of women receiving Lactobacillus crispatus CTV-05 and 50% of those receiving placebo. The most common adverse effects included vaginal discharge or itching or moderate abdominal discomfort.
A novel aspect of this study, the authors say, is the application of quantitative polymerase chain reaction to assess vaginal microbiota after UTI. This enabled them to define sentinel changes in vaginal microbiota with or without the Lactobacillus crispatus CTV-05 probiotic.
Using quantitative polymerase chain reaction to assess L crispatus colonization in women in both study groups, the researchers say, allowed them to distinguish the natural recovery of the vaginal microbiota after UTI, as may have potentially occurred in the placebo group, from specific effects attributable to the probiotic.
What was "striking," the investigators add, was that placebo-treated women often had high concentrations of vaginal L crispatus during follow-up, yet this failed to protect them from rUTI (RR, 1.1; 95% CI, .4 - 3.1). In contrast, women who received Lactobacillus crispatus CTV-05 and achieved high colonization were protected from rUTI (RR, .07; 95% CI, .02 - .3; P < .01).
"Lactin-V after treatment for acute UTI," they conclude, "confers a significant advantage over repopulation of the vaginal microbiota with endogenous L. crispatus."
"Ongoing studies in our group are directed at understanding the mechanisms of protection in vivo and optimizing this prophylactic regimen," they note.

BRCA2 MUTATION LINKED TO BETTER SURVIVAL IN OVARIAN CANCER PATIENTS

Ovarian cancer patients with the BRCA2 gene mutation are more likely to survive their disease than those with the BRCA1 mutation and those without either mutation.
After adjustment for stage, grade, histology and age at diagnosis, BRCA1 carriers showed a modest nonsignificant survival advantage (hazard ratio [HR], 0.84; P = .12). However, BRCA2 carriers showed a marked improvement in survival, compared with noncarriers (HR, 0.57; P = 6 ×10^–4).
The data were presented here at the American Association for Cancer Research 102nd Annual Meeting.
"This is the first solid evidence that BRCA2 carriers show a distinct clinical course from BRCA1 carriers," said lead author Kelly Bolton, MPhil, a predoctoral candidate at the National Cancer Institute.
"Our findings don't have any immediate impact on clinical practice, but they do have important implications for both clinical prediction and trial design — particularly for clinical trials," explained Ms. Bolton.
The next step is to try to understand the mechanism driving these survival differences. "There is some evidence from in vitro work and some retrospective clinical studies that suggest that response to chemotherapy may be different between carriers and noncarriers," she said. "There could also be biological differences that exist that we are not yet aware of between BRCA1 andBRCA2 carriers and noncarriers that are driving this association."
Rare germline mutations in the breast and ovarian cancer predisposition genes BRCA1 and BRCA2 are present in about 10% to 15% of ovarian cancer patients, but are quite uncommon in the general population. Both genes play key roles in DNA damage repair, but appear to have distinct, although often complementary, functions, Ms. Bolton pointed out. Breast and ovarian cancer risks differ between the 2 carrier groups, and mutation-specific effects have been suggested for both.
Possible Treatment Implications
Survival among ovarian cancer patients is quite variable, noted Ellen Goode, PhD, associate professor of epidemiology at the Mayo Clinic in Rochester, Minnesota. "BRCA1 and BRCA2 are 2 genes that increase the risk of ovarian cancer."
"But what hasn't been definitively shown until now is that once you have ovarian cancer, if you are a carrier of one of these genes, that will affect your survival," she told Medscape Medical News. Dr. Goode was not involved in the study.
This study shows that there is a difference in outcome that could lead to variables in treatment. "It could be that we need more tailored chemotherapy, depending on BRCA status," she said.
It is still premature to consider testing all ovarian cancer patients for BRCA status, explained Dr. Goode, but it should be considered on an individual basis. "Testing for BRCA is very expensive, so it is not something that is feasible on a large scale," she said.
"If a woman has a family history of the disease and has already been tested, it is probably something that should be taken into account at this point," she added.
"In terms of chemotherapy regimens, a good next analysis would be to stratify women by carrier status," said Dr. Goode. "In the future, I think that this information will prove useful in terms of treatment."
Survival Advantage for BRCA2 Carriers
In this study, Ms. Bolton and colleagues conducted a large multicenter study to investigate the impact of germline BRCA1 andBRCA2 mutations on ovarian cancer survival.
The cohort consisted of 3531 women with invasive epithelial ovarian cancer, of whom 1178 were BRCA1 carriers, 367 were BRCA2carriers, and 1986 were noncarriers. The team analyzed survival-time data obtained from 24 studies conducted in the United States, Europe, Israel, and Asia. The main analysis excluded patients who had not or who were likely to have not received platinum-based therapy.
BRCA1 and BRCA2 carriers were more likely than noncarriers to present with advanced-stage disease, high-grade tumors, and serous disease. The authors also observed that BRCA1 carriers tended to be younger than noncarriers at diagnosis (P = 2 × 10^–9), and that BRCA2 carriers were slightly older at diagnosis (P = .002).
In terms of tumor stage, grade, and histology, there was no difference between BRCA1 and BRCA2 carriers, but there was a difference in age at diagnosis (P = 2 × 10^–14). In an unadjusted analysis, neither BRCA1 nor BRCA2 carriers differed from noncarriers in overall survival (BRCA1 HR, 1.02; P = .77; BRCA2 HR, 0.89; P = .36). However, after adjustment for baseline characteristics, differences in the 3 groups emerged. For noncarriers, 5-year survival was 36%, for BRCA1 carriers it was 46%, and for BRCA2 carriers it was 61%.
The survival differences that were observed between BRCA1 and BRCA2 carriers could be related to differences in tumor biology or chemosensitivity, the authors note.

Upcoming Talks

I'll be giving at least two talks at conferences this year:

Ancestral Health Symposium; "The Human Ecological Niche and Modern Health"; August 5-6 in Los Angeles. This is going to be a great conference. Many of my favorite health/nutrition writers will be presenting. Organizer Brent Pottenger and I collaborated on designing the symposium's name so I hope you like it.

My talk will be titled "Obesity; Old Solutions to a New Problem." I'll be presenting some of my emerging thoughts on obesity. I expect to ruffle some feathers!

Tickets are going fast so reserve one today! I doubt there will be any left two weeks from now.


TEDx Harvard Law; "Food Policy and Public Health"; Oct 21 at Harvard. My talk is tentatively titled "The American Diet: a Historical Perspective." This topic interests me because it helps us frame the discussion on why chronic disease is so prevalent today, and what are the appropriate public health measures to combat it. This should also be a great conference.

Obesity and the Fluid-in, Fluid-out Therapy for Edema

I recently attended a lecture by Dr. Arya M. Sharma here at the University of Washington. Dr. Sharma is a Canadian clinician who specializes in the treatment of obesity. He gave the UW Science in Medicine lecture, which is a prestigious invited lecture.

He spent a little bit of time pointing out the fallacy behind conventional obesity treatment. He used the analogy of edema, which is an abnormal accumulation of fluid in the body.

Since we know that the amount of fluid contained in the body depends on the amount of fluid entering the body and the amount of fluid leaving the body, the treatment for edema is obvious: drink less, pee more.

Of course, this makes no sense. It doesn't address the underlying cause of edema and it will not help the patient. Yet we apply that exact same logic to fat loss. Since the amount of energy contained in the body (in the form of fat) depends on the amount entering and the amount leaving, the solution is easy: eat less, move more. Well, yes, if you can stick to that program it will cause fat loss. But that's equivalent to telling someone with edema to drink less water. It will cause a loss of fluid, but it won't correct the underlying problem that caused excessive fluid retention in the first place.

For example, if you have edema because your heart isn't pumping effectively (cardiac insufficiency), the heart is the problem that must be addressed. Any other treatment is purely symptomatic and is not a cure.

The same applies to obesity. If you don't correct the alteration in the system that causes an obese person to 'defend' his elevated fat mass against changes*, anything you do is symptomatic treatment and is unlikely to be very effective in the long term. My goal is to develop a method that goes beyond symptomatic treatment and allows the body to naturally return to a lower fat mass. I've been doing a lot of reading and I have a simple new idea that I feel confident in. It also neatly explains the results of a variety of weight loss diets. I've dropped a few hints here and there, but I'll be formally unveiling it in the next couple of months. Stay tuned.


* The body fat homeostasis system. The core element appears to be a negative feedback loop between body fat (via leptin, and insulin to a lesser degree) and the brain (primarily the hypothalamus, but other regions are involved). There are many other elements in the system, but that one seems to set the 'gain' on all the others and guides long-term fat mass homeostasis. The brain is the gatekeeper of both energy intake and energy expenditure, and unconscious processes strongly suggest appropriate levels for both factors according to the brain's perceived homeostatic needs. Those suggestions can be overridden consciously, but it requires a perpetual high degree of discipline, whereas someone who has been lean all her life doesn't require discipline to remain lean because her brain is suggesting behaviors that naturally defend leanness. I know what I'm saying here may seem controversial to some people reading this, because it's contrary to what they've read on the internet or in the popular press, but it's not particularly controversial in my field. In fact, you'll find most of this stuff in general neuroscience textbooks dating back more than 10 years (e.g., Eric Kandel and colleagues, Principles of Neuroscience).

How to Treat Supot-supot or Skin Asthma or Hives?

When I was a child, I and my siblings often suffer from a skin disorder locally called Supot-Supot. This Supot-supot, I later found out is called by the doctors as Skin asthma or Hives.

Hives or skin asthma usually starts with small, almost a dot, red, itchy, raised rashes that may appear in any part of the body. As the rashes are scratched, it grows bigger and bigger until they join together.

Because we live in a barrio my mother thought the cause of the rashes is kulam or a witch’s inflicted disease. Treatment was then for us drinking a concoction of bitter herbal medicines. And for the relief of itch, she would apply Caladryl on our rashes. She would have us dress in black to make the rashes go away (it always puzzled me how). And she would give us a warm bath and make us stay in room with all the windows closed.

I never believed in my mother’s beliefs, because instead of relief, we suffered more with her remedies. So when my daughter suffered from hives, I didn’t do, not even one, of the remedies she treated us with. Instead I went to my pediatrician and I learned that the disease is an allergy, and I learned to properly deal with it.

Hives is very itchy. It’s painfully itchy. A child won’t be able to avoid scratching. And this is not good because the scratching causes the rashes to grow bigger (as it was mentioned earlier). It may as well cause abrasions or bruises which may lead to skin infections.

Causes:

• Hives is an allergic reaction. So it is caused by a wide array of substances. For example:
• Medicine
• Food like shellfish, citrus, fish, eggs, nuts even milk
• Pollen
• Insect bites
• Animal fur/hair like that of cats and dogs

Hives may also be caused by some conditions like:

• Sudden change of temperature
• Stress
• Extreme temperature (either hot or cold)
• Heavy sweating
• Infections
• Diseases

Treatment:

Hives doesn’t need to be treated. The rashes usually go away in a few days. But if it’s causing difficulty in breathing, nausea and dizziness, fever and weakness and if it has persisted for at least more than 4 weeks, it is best to see a doctor.

 Remedy to alleviate the itching:

• Cold compress – you can use water, milk, tea, or boiled guava leaves. When we say cold, it means cool enough, not freezing. Wet a cloth with any of the suggested and cover the rashes with it. Let stand until the coolness disappear.
• Take a cool bath – not necessarily icy cool, just the normal tap water temperature. My pediatrician advised me to add oatmeal. They have this powdered oatmeal in sachets specifically for baths. If you do not have oatmeal you can also use baking soda. ½ box for every bath.
• Aloe Vera Gelly – I have discovered this lotion years ago and it helps a lot. It’s a Forever Living Company product. It’s all natural so it is safe. It also helps cool the rashes.

IMPORTANT:

• Avoid scratching. But since children cannot avoid it, have your child use mittens or soft cloth gloves to help prevent him from bruising himself.
• Have your child wear long clothes to cover the rashes that he may not be able to scratch it with his finger nails.
• Never give your child a warm bath. It will only make the rashes itch more!
• Watch your child for signs of weakness or difficulty in breathing, should these conditions be present, don’t waste time. Bring him to the hospital at once.
• Discover the triggering conditions so as you know to avoid. 

Home Remedy when Kids have Sore Throat

Sore throat is a common health problem among children, but usually is left unattended so it progresses to more severe cases like cough, cold and even flu


Symptoms:


When your child complains of an itchy throat, that's the start
Hoarse voice,
Difficulty in speaking because the throat is sore,
Sometimes fever is present


Remedy:
Have your child drink lots of water, and freshly squeezed citrus juices, preferably with less sugar.
Gargle with lukewarm water mixed with vinegar

US Omega-6 and Omega-3 Fat Consumption over the Last Century

Omega-6 and omega-3 polyunsaturated fats (PUFA) are essential nutrients that play many important roles in the body. They are highly bioactive, and so any deviation from ancestral intake norms should probably be viewed with suspicion. I've expressed my opinion many times on this blog that omega-6 consumption is currently too high due to our high intake of refined seed oils (corn, soybean, sunflower, etc.) in industrial nations. Although it's clear that the quantity of omega-6 and omega-3 polyunsaturated fat have changed over the last century, no one had ever published a paper that attempted to systematically quantify it until last month (1).

Drs. Chris Ramsden and Joseph Hibbeln worked on this paper (the first author was Dr. Tanya Blasbalg and the senior author was Dr. Robert Rawlings)-- they were the first and second authors of a different review article I reviewed recently (2). Their new paper is a great reference that I'm sure I'll cite many times. I'm going to briefly review it and highlight a few key points.

1. The intake of omega-6 linoleic acid has increased quite a bit since 1909. It would have been roughly 2.3% of calories in 1909, while in 1999 it was 7.2%. That represents an increase of 213%. Linoleic acid is the form of omega-6 that predominates in seed oils.

2. The intake of omega-3 alpha-linolenic acid has also increased, for reasons that I'll explain below. It changed from 0.35% of calories to 0.72%, an increase of 109%.

3. The intake of long-chain omega-6 and omega-3 fats have decreased. These are the highly bioactive fats for which linoleic acid and alpha-linolenic acid are precursors. Arachidonic acid, DHA, DPA and EPA intakes have declined. This mostly has to do with changing husbandry practices and the replacement of animal fats with seed oils in the diet.

4. The ratio of omega-6 to omega-3 fats has increased. There is still quite a bit of debate over whether the ratios matter, or simply the absolute amount of each. I maintain that there is enough evidence from highly controlled animal studies and the basic biochemistry of PUFAs to tentatively conclude that the ratio is important. At a minimum, we know that excess linoleic acid inhibits omega-3 metabolism (3, 4, 5, 6). The omega-6:3 ratio increased from 5.4:1 to 9.6:1 between 1909 and 2009, a 78% increase.

5. The biggest factor in both linoleic acid and alpha-linolenic acid intake changes was the astonishing rise in soybean oil consumption. Soybean oil consumption increased from virtually nothing to 7.4% of total calories, eclipsing all sources of calories besides sugar, dairy and grains! That's because processed food is stuffed with it. It's essentially a byproduct of defatted soybean meal-- the second most important animal feed after corn. Check out this graph from the paper:

I think this paper is an important piece of the puzzle as we try to figure out what happened to nutrition and health in the US over the last century.

Welding And Parkinson's, Can Fumes Lead To The Disease?

Fumes produced by welding contain manganese. Manganese is a chemical element that, even at low levels, has been linked to neurologic problems, including Parkinson's disease-like symptoms. New research suggests that workers exposed to welding fumes may be at risk for developing brain damage in an area of the brain also affected inParkinson's disease.

Brad A. Racette, MD, with Washington University School of Medicine in St. Louis and a Fellow with the American Academy of Neurology stated:

"There are over one million workers who perform welding as part of their job functions in the United States. If a link between neurotoxic effects and these fumes were proven, it would have a substantial public health impact for the U.S. workforce and economy."

Almost everyone is exposed to small amounts of manganese, a naturally occurring substance in our air, soil, water and food, daily. If kept in check, the body is able to control manganese levels by expelling extra amounts, but if the intake becomes too great, it can become overwhelming and cause a variety of health problems, including permanent nervous system damage.

What makes manganese so dangerous is that the current safety levels may not be adequate, so people may be taking in dangerous levels of this compound that almost no one is aware of.

The study involved 20 welders with no symptoms of Parkinson's disease, 20 people with Parkinson's disease who were not welders and 20 people who were not welders and did not have Parkinson's.

The welders were recruited from two Midwest shipyards and one metal fabrication company. All participants were given brain PET and MRI scans, motor skills tests and examined by a neurologist who specializes in movement disorders. The welders had an average of 30,000 hours of lifetime welding exposure. Their average manganese levels were found to be two times the upper limits of normal.

Scientists found that welders had an average 11.7% reduction in a marker of dopamine in one area of the brain on PET scans as compared to people who did not weld. Dopamine is a chemical messenger that helps nerve cells communicate and is decreased in specific brain regions in people with Parkinson's disease. The welders' motor skills test scores also showed mild movement difficulties that were about half of that found in the early Parkinson's disease patients.

Racette continues:

"While these changes in the brain and dopamine dysfunction may be an early marker of neuron death related to welding exposure, the damage appeared to be different from those of people with full-fledged Parkinson's disease. MRI scans also revealed brain changes in welders that were consistent with manganese deposits in the brain."

Perhaps most concerning is that permanent damage to the nervous system may occur after exposure to manganese levels that the Environmental Protection Agency (EPA) has noted as safe.

W. R. Wayne Martin, MD from University of Alberta in Edmonton, Alberta, Canada and also a member of the American Academy of Neurology adds:

"Although this study shows that these workers had dopamine dysfunction in the brain, the study authors could not determine whether this was specifically related to manganese. Will these individuals develop full-fledged Parkinson's disease? We can't answer that question based on the study but more research should be done to explore this possibility."

What to do when your child has a flu.

Flu

Flu is not as simple as we thought. It is caused by a virus and it is transferred from one person to another through coughing, sneezing, sharing of eating utensils and having a direct contact with people sick from it. Recovery can be expected in 1-2 weeks time, but there are instances when the infection may develop to life-threatening complications.

Children are mostly at risk because their immune system is not yet as developed as to that of the adults although, it affects all ages.

Symptoms:

• Headache
• Dizziness
• Nausea
• Vomiting
• Weakness or feelings of fatigue
• Muscle aches
• Joint aches
• Sore throat
• Cough
• Cold
• Irritated, watery eyes
• Fever and chills 

What to do when your child is down with fl?

• Give paracetamol to relieve the fever and pain.
• Rest and plenty of water are necessary.
• Monitor the temperature.
• If fever persists and your child is shivering or is having chills, better consult a doctor. 

Caution: 

• Don’t give aspirin to your children.
• Flu is caused by a virus so don’t give your child antibiotics unless your pedia instructs you to. (antibiotics are for bacteria caused diseases)

Prevention:

• Prevention is better than cure. Have your child vaccinated against flu.
• Teach your child to practice good personal hygiene, like proper hand washing. Hand sanitizers are also a great help when hand washing can’t be possible.
• Teach your child to avoid touching his eyes, nose mouth and to cover her mouth and nose when someone sneezes or coughs near or in front of him.

Fat-ten-u

I recently bought the book Food in the United States, 1820s-1890. I came across an ad for an interesting product that was sold in the late 1800s called Fat-ten-u. Check your calendars, it's not April fools day anymore; this is for real. Fat-ten-u was a dietary supplement guaranteed to "make the thin plump and rosy with honest fleshiness of form." I found several more ads for it online, and they feature drawings of despondent, lean women and drawings of happy overweight women accompanied by enthusiastic testimonials such as this:

"FAT-TEN-U FOODS increased my weight 39 pounds, gave me new womanly vigor and developed me finely. My two sisters also use FAT-TEN-U and because of our newly found vigor we have taken up Grecian dancing and have roles in all local productions."

I'm dying to know what was in this stuff, but I can't find the ingredients anywhere.

I find this rather extraordinary, for two reasons:

• Social norms have clearly changed since the late 1800s. Today, leanness is typically considered more attractive than plumpness.
• Women had to make an effort to become overweight in the late 1800s. In 2011, roughly two-thirds of US women are considered overweight or obese, despite the fact that most of them would rather be lean.

A rhetorical question: did everyone count calories in the 1800s, or did their diet and lifestyle naturally promote leanness? The existence of Fat-ten-u is consistent with the idea that our bodies naturally "defended" a lean body composition more effectively in the late 1800s, when our diets were less industrialized. This is supported by the only reliable data on obesity prevalence in the 1890s I'm aware of: body height and weight measurements from over 35,000 Union civil war veterans aged 40-69 years old (1). In that group of Caucasian men, obesity was about 10% of what it is today in the same age group. Whether or not you believe that this sample was representative of the population at large, I can't imagine any demographic in the modern US with an obesity prevalence of 3 percent (certainly not 60 year old war veterans).

Here are two more ads for Fat-ten-u and "Corpula foods" for your viewing pleasure: