Binge Eating and the Sugar Fat Showdown

As so often happens when one takes a closer look at references from one paper or another, one will find a paper far superior to the first. The glass half empty view is one of regret for wasting all that time on the inferior paper. The glass half full - hey, now I have more material for another post. Only I have a stack of about 20 papers in the queue, and these industrious researchers are coming out with more all the time, so material isn't really a problem, even after 170 blog entries.

Let's go for some peppy-ish music today. "What You Know" by Two Door Cinema Club. (right click in new tab)

The great thing about this superior paper is that it is free full text, and well worth taking a look for yourself. Avena et al, Sugar and Fat Bingeing Have Notable Differences in Addictive-like Behavior. It was published in a Journal of Nutrition Symposium, "Food Addiction: Fact or Fiction," and they wrote a convincing work. One caveat - this paper is primarily a review of rat studies. The brand new paper I blogged about last week where they stuck humans in the MRI is one of the first in humans showing neural correlates of addiction with the chocolate milkshakes. So there is definitely more work to be done before we stick a fork in it and declare that we have all the answers. That said, let's visit our rat studies.

People and rats tend to binge on "highly palatable energy-rich food." Binge episodes in research (and in my clinical experience) usually involve episodes of "bread or pasta, followed in frequency by sweets, fatty foods, or salty snacks" (the salty snacks are typically chips or popcorn, so for the most part grains + salt + vegetable oil). Those who prefer to binge on sweet food tend to binge more frequently.

By bingeing, I don't mean hanging out on the couch and eating half a bag of Doritos while watching old episodes of Top Chef. Binge eating in humans has a specific definition - a larger amount of food than normal within a 2 hour period, associated with at least three of the following: 1) eating until uncomfortably full, 2) eating large amounts of food when not hungry, 3) eating more rapidly than normal, 4) eating alone due to embarrassment about the amount of food consumed, 5) feeling disgusted, depressed, or guilty about the amount of food consumed, and 6) distress or anxiety regarding binge eating. Obviously rats don't fill out questionnaires about how they feel about eating, so I'm assuming the rat definition isn't quite so strict (and I would call this issue a problem with animal models of binge eating). I don't know if rats feel guilty about over-consuming.

The human definition is important to remember, because most obese people are not binge eaters. However, binge eaters are far more likely to be obese, and about 1/3 of people in medical treatment for obesity struggle with binge eating. Binge eating is an extreme of the overall issue with obesity in the West - somehow food consumption gets unhooked from the energy in and out regulatory cycles that kept us relatively lean for 10,000 generations - with emotional baggage and addiction to boot.

Back to rats! Many laboratories have done studies with sugar solutions, and they find (in general) that rats will binge on sugar if they are given intermittent access to it, or if they are given sugar after a period of fasting. Typically the sugar solutions are similar to the sugar concentration of soft drinks. Rats who have sugar and their regular diet available all the time tend to eat as much sugar as the restricted rats do, but they don't binge on it. And, importantly, the sugar bingeing rats and the sugar + regular food freely available rats don't tend to get fat. They eat sugar and compensate by eating less rat food.

Contrary to the notion that we don't "binge on fat alone," rats certainly do. Corwin et al. have demonstrated several times that rats who have ready access to their rat food will binge on shortening when it is available for only 2 hours each day. (I myself have never experienced an overwhelming urge to down a bucket of Crisco, come to think of it, and one of the papers notes "humans rarely if ever binge on pure fat.") Proving that at least some diet and obesity researchers have functioning brains and sticktoitiveness, Corwin more or less repeated the experiment with trans-fat free shortening 10 years later, and rats will binge on the new improved Crisco or the old, more deadly version. But, just like the sugar-eating rats, the rats tend to compensate for the extra Crisco binge, at least in these 6 week experiments, by eating less of their regular rat chow.

(Second song - Crystal Vases by The Last Royals)

Another group of rat researchers, leaving no stone unturned, compared intermittently available Crisco (in 2008 I don't know if this was trans-fat Crisco as Corwin's paper in 2007 noted they had trouble getting a hold of trans fat Crisco at the time for their comparison group) to rats given a high fat diet (I couldn't find the exact composition of their high fat diet, but every rat diet I could find at Dyets Inc., where the researchers obtained their rat food, uses soybean oil and corn oil for the fat) every third day for 8 weeks. Both groups would binge on the fat (for one group, pure crisco, for the other, high fat food mix), both groups gained fat (though didn't necessarily gain weight over all). Only the hydrogenated shortening exposed group had changes in leptin levels (their leptin levels increased, which is common with obesity) - this suggests that, at least in rats, hydrogenated vegetable oil has the potential to be more endocrine-disruptive than plain old vegetable oil, but both groups gained body fat, so who knows.

These same researchers also had groups of rats who got the high fat diet every day, a control diet every day, or Crisco every day, and none of the groups (intermittent, constant exposure, control, or not) had any differences in the amount of calories consumed. Only the intermittently exposed rats had bingeing behavior. All of the high fat or Crisco rats (intermittently exposed or not) gained body fat.

Now what we've been waiting for - the sweet-fat mixes. The combination of sweet and fat activates a cornucopia of taste receptors and neuropeptide signaling systems. Sweet-fat combos (some researchers use cookies, in the Avena paper, they used Research Diets #12451 (with sucrose, soybean oil, and I'm guessing industrial lard)), with intermittent access result in bingeing rats again, with the rats consuming 54% of their daily calories during the 2 hour sweet-fat food available window. These rats tend to eat less of their regular rodent chow to compensate, but compared to control groups without sweet-fat access, they actually eat more calories overall. This is the first model that results in rats gaining body weight with bingeing behavior.

SO - in rats, at least, sugar alone causes binges when intermittently available. Vegetable fat and high-vegetabe fat diets will do the same (causing body fat increase without overall weight gain), and the sweet-fat mix (though finally using lard, it is in combination with soybean oil, and industrial lard undoubtedly has a higher omega 6 content than pasture pig lard, which I think is around 12% PUFA) causes bingeing AND weight gain.

A few more interesting things from the Avena paper: Rats given daily intermittent access to sugar will binge in the first hour of sugar access, and when the rats are given a high dose of naloxone (an injectable opiate blocker used in humans for overdoses - you end up with someone who is breathing again but in abrupt opiate withdrawal, so alive, but extremely unhappy and uncomfortable), they exhibit symptoms of opiate withdrawal. Similar signs of rat opiate withdrawal emerge spontaneously in sugar-bingeing rats who are put on a 24 hour fast, no naloxone necessary. And sugar-bingeing rats given a regular diet for 2 weeks will then eat 24% more sugar than ever before after the two weeks without. Sugar-addicted rats who have their fix taken away will also be more anxious, aggressive and will have lower body temperature (a sign of rat stress).

Similar findings (using naloxone again) were seen in rats fed an ad libitum "cafeteria-style" diet with a variety of foods such as cheese, cookies, and chocolate chips. And rats exposed to corn oil will show an increase in dopamine (the feel good chemical) release, and this release will also happen when exposed to just the taste of the oil. Avena's group tried to replicate these findings with a variety of sweet-fat or high fat combinations of rodent chow, but didn't observe the naloxone withdrawal effect, which is interesting.

And, another DING DING moment - Avena's group had found the withdrawal and unhappiness in sugar-bingeing rats after a 24 hour fast. They tried the same thing with rats fed a high fat diet (I'm sure the typical horrid industrial rodent chow), and observed that the rats were not anxious or have indications of distress after 24 hours without food. The researchers felt this was due to sugar stimulating opiate systems, and fat likely not doing so. I also wonder if high-fat rodents were more able to burn ketones so didn't experience uncomfortable fluctuations of energy as a high-carb (again, typically the industrial sugar, corn starch, casein, lactose, soybean oil blah blah blah combination) rat will tend to without eating.

The take-home message? Rats will binge on sugar and vegetable fat, but it is the sugar-fat combination that is the most detrimental to rat body-fat %. It seems that the sugar packs the most addictive punch, while the increase vegetable fat (particularly Crisco, whether trans-fat free or not) in combination with the rest of the industrial diet perhaps causes more metabolic harm.

Does this information apply to humans? Well, there are some differences (i.e. lack of human crisco-diving behavior) and many similarities. And gluten grains seem to be missing in these animal studies, while humans with binge-eating behaviors binge most commonly on bread and pasta.

You know what I think already. Eat real food, avoid the industrial stuff (particularly the vegetable oils), and to really play it safe, avoid the gluten grains too. I don't go too far out of my way to avoid too much sugar, personally - avoiding processed food in general does the trick. I eat fruit if I feel like it (usually bananas or berries, but grapes or apples or oranges are also typical), and usually it ends up being one serving a day. And when I cook recipes with sugar (which isn't all that often), I do cut sugar to 1/2 or 1/4 what the recipe calls for, and I tend to use raw honey or some other specialty ingredient - more because it is expensive and precious and more fun to eat, and easier to savor. I've had my current little bear of raw honey for 6 months. If you are worried about too much fructose, use rice syrup. I don't sweat a little ketchup or tomato paste or balsamic vinegar - it's never that much. Food should be an amazing celebration of nature, not a technological marvel (unless you are enjoying a high-end meal at a molecular gastronomy restaurant). Real food can be enjoyed and celebrated, and it is life-giving and nourishing, never the enemy.

I also have a new post on Psychology Today - Depression Crashed Your Party

Read More..

Other Posts Everywhere

I have another longer look at sugar, vegetable oils, binge eating, addiction, and the brain coming up (chased down some of the references from the papers I mentioned on Saturday, and they do not disappoint), but for today I have a guest post on Mark's Daily Apple, and another Psychology Today post� enjoy!

Your Brain and The Primal Blueprint

Sad Monkeys

And welcome Mark's Daily Apple visitors!  If you think my blog looks interesting, you can start with this post:

Evolutionary Psychiatry, the Key Posts

And if you are looking for something more specific, take a gander at the site Map (has most posts listed by condition (ex. depression or autism,  or nutrient)).

Have fun!

Read More..

A Small Post On The Neurobiology of Binge Eating Disorders

Indulge me for a moment. Here is one of my favorite pieces of music: Chopin's Etude No. 3 in E major. (right click to open in new window). The best youtube quote about it: "Too beautiful to be an etude."

One more indulgence. A quote from A Room with a View by E.M. Forster. For springtime.

From her feet the ground sloped sharply into view, and violets ran down in rivulets and streams and cataracts, irrigating the hillside with blue, eddying round the tree stems, collecting into pools in the hollows, covering the grass with spots of azure foam. But never again were they in such profusion; this terrace was the well-head, the primal source whence beauty gushed out to water the earth.

Standing at its brink, like a swimmer who prepares, was the good man. But he was not the good man that she had expected, and he was alone.

The brain is named in beautiful words, intimidating words, but beautiful nonetheless. We'll start with the animal models of binge eating (1), which seem to have something in common with the human experience. Animals seem more likely to binge in cases of prior food restriction (and the bingeing can continue for long periods after restriction is over), and in periods of anxiety.

Daily binge eating on a "palatable sugar solution or fat diet" will repeatedly release the feel-good chemical dopamine from its home, the nucleus accumbens. Sugar-bingeing rats will have increased dopamine1 receptor binding in the nucleus accumbens, and decreased dopamine2 receptor binding in the dorsal striatum. This pattern is very similar to changes observed with drug dependency. There are also changes in opiate receptor expression in binge eating rats, and if you inject opiate into the nucleus accumbens, it will stimulate binge eating.

Some facts about binge eating in humans - the definition is that someone will eat an "objectively large amount of food" accompanied by feelings of loss of control. 30% of obese individuals attending weight control programs have the disorder. Obese binge eaters will eat significantly more calories than obese nonbinge eaters in order to feel full, or even when asked to eat normally.

In a study on humans, Wang et al discovered that food stimulus significantly increased dopamine signals in binge eaters in the basal areas of the brain, whereas non binge-eaters did not show the same increase.
Previous studies had shown that exposure to "palatable food stimuli" was associated with an increase in striatal dopamine release, and this release was correlated with ratings of "meal pleasantness" following consumption of favorite food. As with the other studies of folks with eating disorders, low dopamine levels (associated with an increase in receptors, to compensate) has been shown to be present in binge eaters.

People with binge eating disorder tend to overeat compulsively and have some impulsivity (also seen in substance abusers), and food is a potent reinforcer of the behavior, and fasting can enhance the rewarding effects (thus my little caveat about IFing and eating disorders).

Here's the evolutionary psychiatry money quote from the Wang article: "Some ingredients in palatable food such as sugar and corn oil can result in impulsive ingestion in patterns reminiscent of those seen with drug intake in addiction." DING DING DING DING.

And the sweet taste of sugar, without the nutritional component, can also induce release of dopamine (um� diet coke addiction, anyone?).

So I don't think I venture far out on a limb to suggest that eating disorders are addictive, or that certain types of extremely palatable food (sugar and corn oil, and in my clinical experience, for some people, wheat) are addictive. Abstinence with support is the tried and true method to help addictions. Hard, though, to get the appropriate sort of universal support when your government (and therefore any trained nutritionist or dietician or doctor of the conventional stamp) is telling you to eat corn oil and grains and carbs to lose weight and to be healthy in general.

Oh! Totally forgot to link yesterday in this blog - a new Psychology Today post is up. Click for me if you please!

Read More..

Eating Disorders, Obesity and Addiction

I've been meaning to do more on eating disorders for a while, but I find the research frustrating.  As do eating disorder researchers - see, within eating disorders even more than in some other areas, the diagnoses proscribed by the DSMIV don't really fit the symptoms most people have.  There are three "official" categories - anorexia nervosa (AN) (restricting eating, underweight, obsessed with body image), bulimia nervosa (BN) (bingeing and purging via vomiting, excessive exercise, or laxatives, typically normal weight or fluctuating weights, body image issues), and eating disorder not otherwise specified (EDNOS)(anyone who seems to have an eating disorder that doesn't quite meet the other criteria).  Most people with eating disorders fall into the last category, simply because many people with primary anorexia also binge and purge in some way, and bulimics will often have periods of restriction.  Even worse, there is an entire category of eating disorders that has no "official" diagnosis, the binge eating disorders (BED) (bingeing without restricting or purging, patients are often overweight but some are normal weight), and it is actually more common than anorexia. (These numbers are approximate as many folks with eating disorders don't seek treatment, but the estimates are that 0.5% of the adult Western population has AN, 1% has BN, and 3% have BED.  There are no estimates for EDNOS.)

When you review the literature for "evidence-based" treatments, there really are none for EDNOS (1), simply because research has focused on AN and BN.  In anorexia, there are a few firm things to recommend - if severely underweight, refeed under supervision, and other treatments don't work particularly well until the starvation is to some extent reversed.  For young people, family therapy is recommended.  In bulimia, there is a particular type of cognitive behavioral therapy that is specific for the disorder and has good evidence base.  

Eating disorders are among the most deadly of psychiatric disorders in the short term (anorexia is probably fatal in 5-10% of cases, though this number is dropping as acute treatment is getting better, whereas BN and EDNOS have a mortality rate of about 3.5%, and people with all the disorders, including BED, have a higher risk of suicide) - but the good news is at 10 year follow-up, between 70-80% of people with the disorders no longer have symptoms.

What is particularly frustrating about eating disorder literature is that no one has a real clue (backed by solid evidence) as to what causes them.  There are some genetic links, some common psychologic features and environmental risk factors, and it is likely that people with low amounts of serotonin and dopamine in certain areas of the brain are more vulnerable to developing eating disorders.  

My own suspicion (speculative, but sensible) is that the combination of societal pressures to be thin and our modern industrial diet's terrible track record of putting on fat lead to very common restricting behaviors, which basically makes everyone a member of a little Minnesota Starvation Experiment, only we are not locked down, so we continuously restrict, worry about exercise, then begin to obsess about food and have anxiety and depressive side effects, then we (quite sensibly) cave in to the evolutionary imperative to eat, regain the weight,  etc. etc.  A particular subset of people, often young women who perhaps face the most societal pressure, will develop extreme behaviors and become eating disordered.  Thus my conjecture is that the industrial food is the problem, and wholesome unprocessed food (get rid of the excess sugar, excess linoleic acid, and gluten grains) a large part of the solution.   My stance is actually as unproven as it is controversial - as many people with eating disorders restrict varieties of food, during recovery it is common practice to teach people to eat "everything in moderation" (though focusing on healthy, nourishing food, of course), so to suggest restricting whole categories of food again without a solid evidence base could be seen as feeding into the disorder.

But there is an issue with "everything in moderation," I think, putting aside the entire "paleolithic" nutritional paradigm and the neolithic agents of disease causing obesity in the first place. And that is that eating disorders are addictive (2).   While some folks with addiction can actually, eventually, moderate their intake of the addictive substance, most people do better, at least for a while, with complete abstinence.  Obviously one cannot completely abstain from food - but if we suspect the neolithic agents as building an addictive cycle neurochemically in the brain (and this is definitely speculation, but an educated guess, I would say), then it would seem that getting rid of them in the diet would be of obvious help.  Once the situation is stabilized, and a more natural and realistic relationship with food and body and diet are adopted, then it would make sense to adopt more moderation to make life easier and less food-obsessed.  But everyone is different - some people get very despondent with the idea that anything is off-limits.  Treating eating disorders like every psychiatric condition requires some common sense, flexibility, and innovation.

Let's get back to my addiction angle for a minute, and, while I'm going to spend some time in a second post focusing on the neurobiology of binge eating, today I'm going to drop "eating disorders" and look at a new paper called Neural Correlates of Food Addiction.  This study is actually about food and obesity in general.

The bottom line in America - 1/3 of adults are obese.  Obesity-related disease is the second-leading cause of preventable death, and most obesity treatments are unsuccessful, with patients regaining all the lost weight within 5 years.  Food and addictive drug use both result in the release of dopamine in the mesolimbic regions of the brain (at least in animal studies), so one gets a sense of "reward" and happiness from eating.  Obese versus lean individuals show greater activation in the addictive behavior centers of the brain in anticipation of receiving "palatable" foods (obesity and food researchers here typically mean sugar and fat and salt - my still-unproven conjecture is that the massive excess of linoleic acid, fructose, and the easy, cheap availability of fatty-grain chips and the like and sweetened grain desserts are the issue, and while a gorgeous bone marrow dressing on a salad and a delicious steak would also light up the reward areas of the brain, it is part of the natural order of things to shut the reward cycle off if our bodies reach a certain level of fat stored on hand.)  And, interestingly, one finds this to be the case in obese individuals and people addicted to drugs - obese people anticipate food intensely, but when the actual food comes, they have less enjoyment (in general, the reward brain areas light up less) than someone who is lean.  The same is true for drug addiction - the brain seems to like the anticipation much more than the actual event.

In the study, 48 young (human) women with an average BMI of 28 were selected from women enrolled in a program "developed to help people maintain a healthy weight on a long term basis."  Those with history of eating disorders, head injury, or current smoking, illicit drug use, or psychiatric diagnosis were excluded.  Each participant was measured and weighed and took some tests assessing their level of food addiction (the research standard is a 25 item Yale Food Addiction Scale.)  The test among these young women had a normal distribution.

Then the participants were put into an MRI for a baseline measurement after fasting 4-6 hours (no caffeine either).  Then the women were exposed to pictures of a chocolate milkshake or a picture of a glass of water for a few seconds.  Thereafter they received one of two "deliveries" - half a milliliter of chocolate milkshake* or a calorie-free tasteless solution meant to mimic saliva.  All of this was randomized - some women got a picture of water then saliva, some milkshake picture then saliva, some water picture then milkshake, etc.   And 40% of the time, no "taste delivery" was made to give the researchers an idea of what a scan would look like without the paired stimulus.  The taste delivery occurred via some sort of tubing system within the MRI scanner itself, which is kind of a neat trick.

Results!  The women (lean or obese) with a high level of food addiction on the scale test showed more activation of brain centers associated with addiction and reward in anticipation with the milkshake picture, and less activation with the actual milkshake.   This is pretty solid human evidence that there are certain people who are truly addicted to chocolate milkshakes.

Interesting tidbits from this study - the addiction scores were not associated with BMI of the participants (average age of 20.8).  However, those with high scores on the addiction scale test were far more likely to have periods of binge eating, emotional eating, and "problematic eating attitudes."   The researchers felt that the young age of the sample might mean that the lean women with a high food addiction score would have increased risk of obesity, as older obese adults tend to have higher food addiction ratings.  I suppose time will tell.

The main problem with the study is that the researchers did not measure hunger in the participants.  Though they all fasted about the same amount of time, some may have been hungrier than others, and hungrier people have greater food reward signals in the brain.  The other limitation I see is the selection in the first place - rather than selecting random young women from a college campus, for example, they chose those enrolled in a healthy eating seminar.  

Well.   What did we learn, really?  "Highly palatable" food can be addictive to certain susceptible individuals.  Usually things are highly palatable because they are somehow good for us.  I have the feeling that in an environment without the neolithic agents of disease, the food reward system would work as planned, just like the sex reward and the exercise reward.  Jack up the system with weird chemicals in excess of anything we ever experienced in evolution - like heroin, tobacco, or ho-hos, and some people will develop a problem.

  

* Obesity researcher milkshake recipe:  4 scoops Haagen-Dazs vanilla ice cream, 1.5 cups of 2% milk, and 2 tbs of Hershey's chocolate syrup.  Personally I would recommend using some variety of artesian or homemade reduced sugar chocolate ice cream and whole milk without the syrup ;-)  Also whipped cream and chocolate shavings on top.

Read More..

Zombieland 2

Go forth and prosper, new Psychology Today post!

Zombieland 2 - Early Mother's Day Edition

Read More..

Spring Fever

Updated Zombieland for Psychology Today - go over there and take a look, will you?  I know I should have waited for the week day, but I have Zombieland II to do also, and when I do get a relative moment of peace around here, I do like to take advantage.

We even had a chance to go outside, where my daughter's little plastic boat was found unhappily waiting for the snow to melt.  A turkey loped through the yard this morning, and you can see his or her track in the upper left.  We have a large family of wild turkeys in the neighborhood.

Read More..

That O6/O3 Ratio, Still Important

Oof.  I'm tired.  Oldest child has a spiky fever of unknown origin (FUO in the medical speak) and youngest child is nearly two and tiring by default.  I get these rather silly emails from babysomethingorother telling me about her 23 month old expected developmental stages.  This week's was about her learning to throw things.  Well, she's been throwing things with gusto for quite a while, babysomethingorother.  She also fingerpaints in yogurt on the refrigerator if I allow it.  I guess she's advanced.  Must be the pasture butter and salmon.  They are both sleeping now and thus, a post.

Well.  The lovely Victoria sent me this new paper last week.  If you can't be bothered to click, basically it is a PUFA and dementia and depression paper.  Dementia is bad, depression is bad.  Those with an early form of dementia called mild cognitive impairment who are also depressed are more likely to progress to severe dementia.  Is there a common biologic mechanism?  (Me: YES OF COURSE.  It's called inflammation.  Also, crappy brain energetics.  Researchers:  Let's take a calm and compelling look at the evidence, particularly as regards to the omega 3 and omega 6 fatty acids and the resultant suspected increase in vulnerability to inflammation.  Me: Sigh.  Yes, let's.)

Okay - so if you look at PUFA O3:O6 in the red blood cell plasma membranes, which is felt to be a marker of the bodily PUFA ratio in general, in general (but not always), studies have shown that a lower Omega 3 DHA is associated with depression (in young and old populations) and worsening dementia.  In this study, red blood cell PUFA status was compared between healthy controls and older people with mild cognitive impairment and also with depressive symptoms.

The methods section is tedious but important but we'll skip in my article to the results.  79 volunteers, 50 with mild cognitive impairment and 29 healthy controls.  Anyone on an omega 3 supplement was excluded (3 people total - in Australia something like 50% of the pregnant moms were excluded from the omega 3 study because they were already on supplements.  I guess the older crowd is not so proactive. )

It's complicated, but basically higher levels of n-6 PUFAs were associated with poorer cognitive performance, as well as lower levels of n-3 DHA and EPA.  Similar results were found for "self-reported mental health."  Also "Bodily Pain."  Many of these were linear relationships - basically the more inflammatory omega 6 you have glopping around in your bod, the more you are likely to be depressed, cognitively impaired, and in Bodily Pain.  The researchers go so far as to recommend that older adults have their RBC O3:O6 ratio measured to establish a risk profile for mild cognitive impairment or depression.

I would say - this is an actionable ratio, folks!  Can the corn chips and industrial salad dressings!  There is some evidence that the omega 6 metabolism pathway is overactive in depressed folks with early dementia.  All the more reason not to feed the O6 machine.  In the brain, we are supposed to have a crapload of DHA.  If we don't have enough DHA, it is replaced with a different looking and different functioning omega -derived AA.

Last year my beloved Texas Longhorns football team played for the national championship.  Our tried and true senior quarterback was taken out early in the game in a freak accident, to be replaced by an untried greenhorn.  We lost.  Our freshman replacement quarterback was well-intentioned but in the wrong place at the wrong time.  He just wasn't the same.

"Previous research has shown associations between better mental and physical health and a more varied diet in older age."  I'm not exactly sure what that means.  I think it means eat some fish already.

Read More..