The Twinkie Diet for Fat Loss

The Experiment

I've received several e-mails from readers about a recent experiment by nutrition professor Mark Haub at Kansas State university (thanks to Josh and others). He ate a calorie-restricted diet in which 2/3 of his calories came from junk food: Twinkies, Hostess and Little Debbie cakes, Dorito corn chips and sweetened cereals (1). On this calorie-restricted junk food diet (800 calorie/day deficit), he lost 27 pounds in two months.

Therefore, junk food doesn't cause fat gain and the only thing that determines body fatness is how much you eat and exercise. Right?

Discussion

Let's start with a few things most people can agree on. If you don't eat any food at all, you will lose fat mass. If you voluntarily force-feed yourself with a large excess of food, you will gain fat mass, whether the excess comes from carbohydrate or fat (2). So calories obviously have something to do with fat mass.

But of course, the situation is much more subtle in real life. Since a pound of body fat contains roughly 3,500 calories, eating an excess of 80 calories per day (1 piece of toast) should lead to a weight gain of 8 lbs of fat per year. Conversely, if you're distracted and forget to eat your toast, you should lose 8 lbs of fat per year, which would eventually be dangerous for a lean person. That's why we all record every crumb of food we eat, determine its exact calorie content, and match that intake precisely with our energy expenditure to maintain a stable weight.

Oh wait, we don't do that? Then how do so many people maintain a stable weight over years and decades? And how do wild animals maintain a stable body fat percentage (except when preparing for hibernation) even in the face of food surpluses? How do lab rats and mice fed a whole food diet maintain a stable body fat percentage in the face of literally unlimited food, when they're in a small cage with practically nothing to do but eat?

The answer is that the body isn't stupid. Over hundreds of millions of years, we've evolved sophisticated systems that maintain "energy homeostasis". In other words, these systems act to regulate fat mass and keep it within the optimal range. The evolutionary pressures operating here are obvious: too little fat mass, and an organism will be susceptible to starvation; too much, and an organism will be less agile and less efficient at locomotion and reproduction. Energy homeostasis is such a basic part of survival that even the simplest organisms regulate it.

Not only is it clear that we have an energy homeostasis system, we even know a thing or two about how it works. Early studies showed that lesioning a part of the brain called the ventromedial hypothalamus causes massive obesity (3; this is also true in humans, when a disruption results from cancer). Investigators also discovered several genetic mutations in rats and mice that result in massive obesity*. Decades-long research eventually demonstrated that these models have something in common: they all interfere with an energy homeostasis circuit that passes information about fat mass to the hypothalamus via the hormone leptin.

The leptin system is a classic negative feedback loop: the more fat mass accumulates, the more leptin is produced. The more leptin is produced, the more the hypothalamus activates programs to reduce hunger and increase energy expenditure, which continues until fat mass is back in the optimal range. Conversely, low fat mass and low leptin lead to increased hunger and energy conservation by this same pathway**.

So if genetic mutants can become massively obese, I guess that argues against the idea that voluntary food intake and energy expenditure are the only determinants of fat mass. But a skeptic might point out that these are extreme cases, and such mutations are so rare in humans that the analogy is irrelevant.

Let's dig deeper. There are many studies in which rodents are made obese using industrial high-fat diets made from refined ingredients. The rats eat more calories (at least in the beginning), and gain fat rapidly. No big surprise there. But what may come as a surprise to the calorie counters is that rodents on these diets gain body fat even if their calorie intake is matched precisely to lean rodents eating a whole food diet (4, 5, 6). In fact, they sometimes gain almost as much fat as rodents who are allowed to eat all the industrial food they want. This has been demonstrated repeatedly.

How is this possible? The answer is that the calorie-matched rats reduce their energy expenditure to a greater degree than those that are allowed free access to food. The most logical explanation for this behavior is that the "set point" of the energy homeostasis system has changed. The industrial diet causes the rodents' bodies to "want" to accumulate more fat, therefore they will accomplish that by any means necessary, whether it means eating more, or if that's not possible, expending less energy. This shows that a poor diet can, in principle, dysregulate the system that controls energy homeostasis.

Well, then why did Dr. Haub's diet allow him to lose weight? The body can only maintain body composition in the face of a calorie deficit up to a certain point. After that, it has no choice but to lower fat mass. It will do so reluctantly, at the same time increasing hunger, and reducing lean mass***, muscular strength and energy dedicated to tissue repair and immune function. However, I hope everyone can agree that a sufficient calorie deficit can lead to fat loss regardless of what kind of food is eaten. Dr. Haub's 800 calorie deficit qualifies. I think only a very small percentage of people are capable of maintaining that kind of calorie deficit for more than a few months, because it is mentally and physically difficult to fight against what the hypothalamus has decided is in your best interest.

My hypothesis is that, in many people, industrial food and an unnatural lifestyle lead to gradual fat gain by dysregulating the energy homeostasis system. This "breaks" the system that's designed to automatically keep our fat mass in the optimal range by regulating energy intake, energy expenditure and the relative partitioning of energy resources between lean and fat tissue. This system is not under our conscious control, and it has nothing to do with willpower.

I suspect that if you put a group of children on this junk food diet for many years, and compared them to a group of children on a healthy diet, the junk food group would end up fatter as adults. This would be true if neither group paid any attention to calories, and perhaps even if calorie intake were identical in the two groups (as in the rodent example). The result of Dr. Haub's experiment does not contradict that hypothesis.

So do calories matter? Yes, but in a healthy person, all the math is done automatically by the hypothalamus and energy balance requires no conscious effort. In 2010, many people have already accumulated excess fat mass. How that may be sustainably lost is another question entirely, and a more challenging one in my opinion. As they say, an ounce of prevention is worth a pound of cure. There are many possible strategies, with varying degrees of efficacy that depend highly on individual differences, but I think overall the question is still open. I discussed some of my thoughts in a recent series on body fat regulation (7, 8, 9, 10, 11).


* ob/ob and db/db mice. Zucker and Koletsky rats. Equivalent mutations in humans also result in obesity.

** Via an increase in muscular efficiency and perhaps a decrease in basal metabolism. Thyroid hormone activity drops.

*** Loss of muscle, bone and connective tissue can be compensated for by strength training during calorie restriction. Presumed loss of other non-adipose tissues (liver, kidney, brain, etc.) is probably not affected by strength training.

Read More

Observations from France

I recently got back from a trip to the UK and France visiting family and friends. It was great to see everyone, eat great food and even do some unexpected foraging (chestnuts, mushrooms, walnuts, blackberries). French people are in better general health than most industrialized nations. The obesity, diabetes and heart disease rates are all considerably lower than in the US, although still much higher than in non-industrial cultures. Here are a few of my observations about French food:

1. The French diet generally contains a lot of fat, mostly from traditional animal sources such as dairy and pork fat. Industrial seed oils have crept into the diet over the course of the 20th century, although not to the same degree as in most affluent nations. People seem to think that eating a lot of fat is unhealthy, particularly the younger generation, but they do it anyway. I had dinner with my family at a traditional restaurant in Lyon (a "bouchon Lyonnais" called Stepharo) last week. Before we ordered, they immediately brought out crispy fried chunks of pork skin and fat (I'm not claiming this is healthy!). The entree was a salad: a bed of lettuce piled high with chicken livers, herring, and "pig's feet". The pigs feet were essentially gobs of pork fat. It was a very good meal that I'll continue describing later in the post. I think it's worth pointing out that Lyon is in Southern France. Is this the "Mediterranean diet"?
   
2. French people eat organs. Yes, they never got the memo that muscle meat is the only edible tissue. A typical butcher or even grocery store will have liver, tripe, kidney and blood sausage on full display next to the meat. If you want to make a French person angry, try selling them a chicken or a rabbit without the liver, gizzard and heart. The main course at Stepharo was a large "andouilette", or tripe sausage, baked in mustard sauce. This was a typical traditional restaurant, not a hangout for gastronauts.
   
3. French people fiercely defend the quality of their food. Have you heard of the abbreviation AOC? It stands for "Appellation d’Origine Contrôlée", or controlled designation of origin. A familiar example is Champagne, which has the AOC label. You can't call your sparkling wine Champagne unless it comes from the region Champagne. However, that's only half the story. AOC also designates a specific, traditional production method, in this case called the "méthode champenoise." The AOC label can apply to a variety of food products, including wine, butter, cheese, honey, mustard and seafood, and is a guarantee of quality and tradition. 44 cheeses currently have the AOC designation, and these are commonly available in markets and grocery stores throughout the country (1). These are not fancy products that only the wealthy can afford-- many of them are quality foods that are accessible to nearly everyone. AOC defines many aspects of cheese production, often requiring a minimum amount of pasture time and specifying livestock breeds. The US has a few products that are regulated in a similar fashion, such as Bourbon whiskey, but generally we are far behind in assuring food quality and transparency.
4. French people cook. There is less outsourcing of food processing in France, for several reasons. One reason is that restaurants are generally expensive. That trend is changing however.

I don't think the French diet is optimal by any means. They eat a lot of white flour, some sugar, seed oils and other processed foods. But I do think the French diet has many good qualities, and it certainly poses a number of problems for the mainstream concept of healthy food. Hence the "French paradox."

Read More

Obesity and the Brain

Nature Genetics just published a paper that caught my interest (1). Investigators reviewed the studies that have attempted to determine associations between genetic variants and common obesity (as judged by body mass index or BMI). In other words, they looked for "genes" that are suspected to make people fat.

There are a number of gene variants that associate with an increased or decreased risk of obesity. These fall into two categories: rare single-gene mutations that cause dramatic obesity, and common variants that are estimated to have a very small impact on body fatness. The former category cannot account for common obesity because it is far too rare, and the latter probably cannot account for it either because it has too little impact*. Genetics can't explain the fact that there were half as many obese people in the US 40 years ago. Here's a wise quote from the obesity researcher Dr. David L. Katz, quoted from an interview about the study (2):

Let us by all means study our genes, and their associations with our various shapes and sizes... But let's not let it distract us from the fact that our genes have not changed to account for the modern advent of epidemic obesity -- our environments and lifestyles have.

Exactly. So I don't usually pay much attention to "obesity genes", although I do think genetics contributes to how a body reacts to an unnatural diet/lifestyle. However, the first part of his statement is important too. Studying these types of associations can give us insights into the biological mechanisms of obesity when we ask the question "what do these genes do?" The processes these genes participate in should be the same processes that are most important in regulating fat mass.

So, what do the genes do? Of those that have a known function, nearly all of them act in the brain, and most act in known body fat regulation circuits in the hypothalamus (a brain region). The brain is the master regulator of body fat mass. It's also the master regulator of nearly all large-scale homeostatic systems in the body, including the endocrine (hormone) system. Now you know why I study the neurobiology of obesity.


* The authors estimated that "together, the 32 confirmed BMI loci explained 1.45% of the inter-individual variation in BMI." In other words, even if you were unlucky enough to inherit the 'fat' version of all 32 genes, which is exceedingly unlikely, you would only have a slightly higher risk of obesity than the general population.

Read More

Vacation

I'll be out of town until the beginning of November, so I won't be responding to comments or e-mails for a while. I'm going to set up a post or two to publish while I'm gone.

As an administrative note, I get a number of e-mails from blog readers each day. I apologize that I can't respond to all of them, as it would require more time than I currently have to spare. The more concise your message, the more likely I'll read it and respond. Thanks for your understanding.

Read More

Sleep Post Correction

An astute commenter pointed out that I misread the numbers in the paper on sleep and fat loss. I wrote that out of the total 3.0 kg lost, the high-sleep group lost 2.4 kg as fat, and the low-sleep group lost 1.4 kg of fat out of 2.9 kg total.

In fact, the high-sleep group lost 1.4 out of 2.9 kg as fat, and the low-sleep group lost 0.6 out of 3.0 kg as fat. So I got the numbers all mixed up. Sorry for the mistake. The main point of the post still stands though: sleep deprivation negatively influences body composition.

The correct numbers are even more interesting than the ones I made up. Even in the high-sleep group, nearly half the body weight lost by simple calorie restriction was lean mass. That doesn't make calorie restriction look very good!

In the sleep-deprived group, 80% of the weight lost by calorie restriction came out of lean mass. Ouch!

That illustrates one of the reasons why I'm skeptical of simple calorie restriction as a means of fat loss. When the body "wants" to be fat, it will sacrifice lean mass to preserve fat tissue. For example, the genetically obese Zucker rat cannot be starved thin. If you try to put it on a severe calorie-restricted diet, it will literally die fat because it will cannibalize its own lean mass (muscle, heart, brain, etc.) to spare the fat. That's an extreme example, but it illustrates the point.

The key is not only to balance energy intake with expenditure (which the brain does automatically when it's working correctly), but to allocate energy appropriately to lean and fat mass.

Read More

The Big Sleep

This blog usually focuses on diet, because that's my specialty. But if you want Whole Health, you need the whole package: a diet and lifestyle that is broadly consistent with our evolutionary heritage. I think we all know that on some level, but a recent paper has reminded me of it.

I somehow managed to get on the press list of the Annals of Internal Medicine. That means they send me embargoed papers before they're released to the general public. That journal publishes a lot of high-impact diet studies, so it's a great privilege for me. I get to write about the studies, and publish my analysis at the time of general release, which is the same time the news outlets publish their stories.

One of the papers they sent me recently is a fat loss trial with an interesting twist (1; see below). All participants were told to eat 10% fewer calories that usual for two weeks, however half of them were instructed to sleep for 8 and a half hours per night, and the other half were instructed to sleep for 5 and a half hours*. The actual recorded sleep times were 7:25 and 5:14, respectively.

Weight loss by calorie restriction causes a reduction of both fat and lean mass, which is what the investigators observed. Both groups lost the same amount of weight. However, 80% of the weight was lost as fat in the high-sleep group (2.4/3.0 kg lost as fat), while only 48% of it was lost as fat in the low-sleep group (1.4/2.9 kg lost as fat). Basically, the sleep-deprived group lost as much lean mass as they did fat mass, which is not good!

There are many observational studies showing associations between insufficient sleep, obesity and diabetes. However, I think studies like that are particularly vulnerable to confounding variables, so I've never known quite what to make of them. Furthermore, they often show that long sleep duration associates with poor health as well, which I find highly unlikely to reflect cause and effect. I discussed one of those studies in a post a couple of years ago (2). That's why I appreciate this controlled trial so much.

Another sleep restriction trial published in the Lancet in 1999 showed that restricting healthy young men to four hours of sleep per night caused them to temporarily develop glucose intolerance, or pre-diabetes (3).

Furthermore, their daily rhythm of the hormone cortisol became abnormal. Rather than the normal pattern of a peak in the morning and a dip in the evening, sleep deprivation blunted their morning cortisol level and enhanced it in the evening. Cortisol is a stress hormone, among other things, and its fluctuations may contribute to our ability to feel awake in the morning and ready for bed at night.

The term "adrenal fatigue", which refers to the aforementioned disturbance in cortisol rhythm, is characterized by general fatigue, difficulty waking up in the morning, and difficulty going to sleep at night. It's a term that's commonly used by alternative medical practitioners but not generally accepted by mainstream medicine, possibly because it's difficult to demonstrate and the symptoms are fairly general. Robb Wolf talks about it in his book The Paleo Solution.

The investigators concluded:

Sleep debt has a harmful impact on carbohydrate metabolism and endocrine function. The effects are similar to those seen in normal ageing and, therefore, sleep debt may increase the severity of age-related chronic disorders.

So there you have it. Besides making us miserable, lack of sleep appears to predispose to obesity and diabetes, and probably sets us up for the Big Sleep down the line. I can't say I'm surprised, given how awful I feel after even one night of six hour sleep. I feel best after 9 hours, and I probably average about 8.5. Does it cut into my free time? Sure. But it's worth it to me, because it allows me to enjoy my day much more.

Keep your room as dark as possible during sleep. It also helps to avoid bright light, particularly in the blue spectrum, before bed (4). "Soft white" bulbs are preferable to full spectrum in the evening. If you need to use your computer, dim the monitor and adjust it to favor warm over cool colors. For people who sleep poorly due to anxiety, meditation before bed can be highly effective. I posted a tutorial here.

1. Nedeltcheva, AV et al. "Insufficient Sleep Undermines Dietary Efforts to Reduce Adiposity." Annals of Internal Medicine. 2010. Advanced publication.


* The study was a randomized crossover design with a 3 month washout period, which I consider a rigorous design. I think the study overall was very clever. The investigators used calorie restriction to cause rapid changes in body composition so that they could see differences on a reasonable timescale, rather than trying to deprive people of sleep for months and look for more gradual body fat changes without dietary changes. The latter experiment would have been more interesting, but potentially impractical and unethical.

Read More

Potatoes and Human Health, Part III

Potato-eating Cultures: the Quechua

The potato is thought to have originated in what is now Peru, on the shores of lake Titicaca. Native Peruvians such as the Quechua have been highly dependent on the potato for thousands of years. A 1964 study of the Quechua inhabitants of Nuñoa showed that they obtained 74% of their calories from potatoes (fresh and chuños), 10% from grains, 10% from Chenopodia (quinoa and cañihua), and 4% from animal foods. Total energy intake was 3,170 calories per day (1).

In 2001, a medical study of rural Quechua men reported an average body fat percentage of 16.4% (2). The mean age of the volunteers was 38. Body fat did increase slowly with age in this population, and by age 65 it was predicted to be about 20% on average. That's below the threshold of overweight, so I conclude that most men in this population are fairly lean, although there were a few overweight individuals.

In 2004, a study in rural Quechua women reported a body fat percentage of 31.2% in volunteers with a mean age of 35 (3). Body fat percentage was higher in a group of Quechua immigrants to the Peruvian capital of Lima. Among rural women, average fasting insulin was 6.8 uIU/mL, and fasting glucose was 68.4 mg/dL, which together suggest good insulin sensitivity and glucose control (4). Insulin and glucose were considerably lower in the rural group than the urban group. Blood pressure was low in both groups. Overall, this suggests that overweight is common among Quechua women.

Rural Quechua are characteristically short, with the average adult man standing no more than 5' 2" (2). One might be tempted to speculate that this reflects stunting due to a deficient diet. However, given the fact that nearly all non-industrial populations, including contemporary hunter-gatherers, are short by modern standards, I'm not convinced the Quechua are abnormal. A more likely explanation is that industrial foods cause excessive tissue growth in modern populations, perhaps by promoting overeating and excessive insulin and IGF-1 production, which are growth factors. I first encountered this hypothesis in Dr. Staffan Lindeberg's book Food and Western Disease.

I don't consider the Quechua diet to be optimal, but it does seem to support a reasonable level of metabolic health. Rural Quechua men subsisting on potatoes are relatively lean, while women are often overweight, though less overweight than urban Quechua who eat fewer potatoes. Unfortunately, I don't have more detailed data on other aspects of their health, such as gastrointestinal health.

Potato-eating Cultures: the Aymara


The Aymara are another potato-dependent people of the Andes, who span Peru, Bolivia and Chile. The first paper I'll discuss is titled "Low Prevalence of Type II Diabetes Despite a High Body Mass Index in the Aymara Natives From Chile", by Dr. Jose Luis Santos and colleagues (5). In the paper, they show that the prevalence of diabetes in this population was 1.5%, and the prevalence of pre-diabetes was 3.6%. The prevalence of both remained low even in the elderly. Here's a comparison of those numbers with figures from the modern United States (6):

That's quite a difference! The prevalence of diabetes in this population is low, but not as low as in some cultures such as the Kitavans (7, 8).

Now to discuss the "high body mass index" referenced in the title of the paper. The body mass index (BMI) is the relation between height and weight, and often, but not always, reflects fatness. The average BMI of this population was 24.9, which is very close to the cutoff between normal and overweight (25).

Investigators were surprised to find such a low prevalence of diabetes in this population, despite their apparent high prevalence of overweight. Yet if you've seen pictures of rural native South Americans, you may have noticed they're often built short and thick, with wide hips and big barrel chests. Could this be confounding the relationship between BMI and body fatness? To answer that question, I found another paper that estimated Aymara body fat using skinfold measurements (9). That study reported that both men and women remained relatively lean throughout life (ages 4-65), with only two of 23 subjects classified as overweight on the basis of body fat percentage, and none classified as obese.

Back to the first paper. In this Aymara group, blood pressure was on the high side. Serum cholesterol was also a bit high for a traditionally-living population, but still lower than most modern groups (~188 mg/dL). I find it very interesting that the cholesterol level in this population that eats virtually no fat was the same as on Tokelau, where nearly half of calories come from highly saturated coconut fat (10, 11). Fasting insulin is also on the high side in the Aymara, which is also interesting given their good glucose tolerance and low prevalence of diabetes.  This could be related to differences in the measurement assay rather than a true difference in fasting insulin, since these assays were often not standardized between studies.

Together, this shows that a lifetime of high-carbohydrate, high-glycemic food does not necessarily lead to overweight or metabolic problems in the context of a traditional diet and lifestyle.

Potato-eating Cultures: the Irish

Potatoes were introduced to Ireland in the 17th century. They were well suited to the cool, temperate climate, and more productive than any other crop. By the early 18th century, potatoes were the main source of calories, particularly for the poor who ate practically nothing else. In 1839, the average Irish laborer obtained 87% of his calories from potatoes (12). In 1845, the potato blight Phytophthora infestans struck, decimating potato plantations nationwide and creating the Great Famine.

There isn't much reliable information on the health status of the Irish prior to the famine, besides reports of vitamin A deficiency symptoms (13) due to the fact that neither of the primary articles of diet, potatoes and buttermilk, provide significant vitamin A. However, the Irish at the time had a very high fertility rate, and anecdotal reports described them as healthy and attractive (14):

As far as fecundity is concerned, the high nutritional value of the potato diet might have played a significant role, but little supportive evidence has been presented so far... What is known is that the Irish in general and Irish women in particular were widely described as healthy and good-looking. Adam Smith's famous remark that potatoes were "peculiarly suitable to the health of the human constitution" can be complemented with numerous observations from other contemporary observers to the same effect.

Controlled Feeding Studies

Starting nearly a century ago, a few researchers decided to feed volunteers potato-only diets to achieve various research objectives. The first such experiment was carried out by a Dr. M. Hindhede and published in 1913 (described in 15). Hindhede's goal was to explore the lower limit of the human protein requirement and the biological quality of potato protein. He fed three healthy adult men almost nothing but potatoes and margarine for 309 days (margarine was not made from hydrogenated seed oils at the time), all while making them do progressively more demanding physical labor. They apparently remained in good physical condition. Here's a description of one of his volunteers, a Mr. Madsen, from another book (described in 16; thanks to Matt Metzgar):

In order to test whether it was possible to perform heavy work on a strict potato diet, Mr. Madsen took a place as a farm laborer... His physical condition was excellent. In his book, Dr. Hindhede shows a photograph of Mr. Madsen taken on December 21st, 1912, after he had lived for almost a year entirely on potatoes. This photograph shows a strong, solid, athletic-looking figure, all of whose muscles are well-developed, and without excess fat. ...Hindhede had him examined by five physicians, including a diagnostician, a specialist in gastric and intestinal diseases, an X-ray specialist, and a blood specialist. They all pronounced him to be in a state of perfect health.

Dr. Hindhede discovered that potato protein is high quality, providing all essential amino acids and high digestibility. Potato protein alone is sufficient to sustain an athletic man (although that doesn't make it optimal). A subsequent potato feeding study published in 1927 confirmed this finding (17). Two volunteers, a man and a woman, ate almost nothing but potatoes with a bit of lard and butter for 5.5 months. The man was an athlete but the woman was sedentary. Body weight and nitrogen balance (reflecting protein gain/loss from the body) remained constant throughout the experiment, indicating that their muscles were not atrophying at any appreciable rate, and they were probably not putting on fat. The investigators remarked:

The digestion was excellent throughout the experiment and both subjects felt very well. They did not tire of the uniform potato diet and there was no craving for change.

In one of his Paleo Diet newsletters titled "Consumption of Nightshade Plants (Part 1)", Dr. Loren Cordain referenced two feeding studies showing that potatoes increase the serum level of the inflammatory cytokine interleukin-6 (22, 23). However, one study was not designed to determine the specific role of potato in the change (two dietary factors were altered simultaneously), and the other used potato chips as the source of potato. So I don't find these studies particularly relevant to the question at hand.

Just yesterday, Chris Voigt of the Washington State Potato Commission embarked on his own n=1 potato feeding experiment as a way to promote Washington state potatoes. He'll be eating nothing but potatoes and a little fat for two months, and getting a full physical at the end. Check out his website for more information and updates (18). Mr. Voigt has graciously agreed to a written interview with Whole Health Source at the end of his experiment. He pointed out to me that the Russet Burbank potato, the most popular variety in the United States, is over 135 years old. Stay tuned for more interesting facts from Mr. Voigt in early December.

Observational Studies

With the recent interest in the health effects of the glycemic index, a few studies have examined the association between potatoes and health in various populations. The results are all over the place, with some showing positive associations with health, and others showing negative associations (19, 20, 21). As a whole, I find these studies difficult to interpret and not very helpful.

Anecdotes

Some people feel good when they eat potatoes. Others find that potatoes and other members of the nightshade family give them digestive problems, exacerbate their arthritis, or cause fat gain. I haven't encountered any scientific research to substantiate claims that nightshades aggravate arthritis or other inflammatory conditions. However, that doesn't necessarily mean there aren't individuals who are sensitive. If potatoes don't agree with you, by all means avoid them.

The Bottom Line

You made it to the end! Give yourself a pat on the back. You deserve it.

In my opinion, the scientific literature as a whole, including animal and human studies, suggests rather consistently that potatoes can be a healthy part of a varied diet for most people, and they probably do not generally promote digestive problems, fat gain, or metabolic dysfunction.  Nevertheless, I wouldn't recommend eating nothing but potatoes for any length of time. If you do choose to eat potatoes, follow these simple guidelines:

• Don't eat potatoes that are green, sprouting, blemished, or damaged
• Store them in a cool, dark place. They don't need to be refrigerated but it will extend their life
  
• Peel them before eating if you rely on them as a staple food
  

Enjoy your potatoes!

Read More