Cognitive Decline and the Mediterranean Diet

I have previous posted on some of the research related to beneficial effects of a Mediterranean style diet on health.  In one post I summarized some of the quantities of food types in those judged to have a high rating for the diet.

A recent study by Tangney and colleagues looked at the rate of cognitive decline in a prospective study of elderly adults in Chicago, Illinois.  The study retrospectively judged the diet of participants for characteristics consistent with a Mediterranean diet.  The exact scoring sheet is not included in the manuscript but based on the data provided and other resources, I have attempted to summarize the rating in the spreadsheet below.

Before looking at the rating system, the study results of note include:

• Subjects were rated on compliance with the Mediterranean Diet and another diet rating for compliance with the USDA food pyramid model
• White subjects scored higher on compliance with the Mediterranean diet while black subjects scored higher on the USDA food pyramid model
• Higher scores on the Mediterranean diet were correlated with a slower rate of cognitive decline over time (cognitive decline was judged based on a composite score of a memory test, the Minimental Status Exam and a digit symbol substitution test)

Looking in more detail at this current study, the highest tertile (highest third) in the Mediterranean diet scored 30-45 on the Mediterranean average weekly diet score. (There was some score adjustment for total calorie intake it the study).  The rating includes 11 categories rated from 0-5 on each item for a maximum of 55 points.  The study looked at two different ratings for alcohol intake.  One looked only at alcohol intake and one looked at total alcohol intake. (Use only one of the two rating for item 11, not both).  Both low and high consumption of alcohol is rated lower on the scale than a consumption of 1-2 drinks per day.  Interestingly, a slower rate of cognitive decline was found in the present study when either red wine or total alcohol was used.

The amount of weekly servings for cereals/whole grains and vegetables looks a little overwhelming.  But four slices of whole grain bread per day by itself would put you in the 4 rated for cereals/pasta/whole grains.  You really only need a top score of 5 in 6 categories to reach what was found as the top third in a U.S. sample.  If you throw in a couple of days per week without red meat you can reach a 3 in the red meat category (I hate to make this recommendation since my father raised cattle in Nebraska). 


So looking at the scoring system used in this study helps put the diet in better perspective.  Many people are probably scoring mid-range on the Mediterranean diet but with a few adjustments could significant improve their compliance with the diet.


Photo of WGC Accenture winner Luke Donald at 2010 PGA Championship courtesy of Yates Photography. 


Spreadsheet summary scale adapted from manuscript by author.


Tangney CC, Kwasny MJ, Li H, Wilson RS, Evans DA, & Morris MC (2011). Adherence to a Mediterranean-type dietary pattern and cognitive decline in a community population. The American journal of clinical nutrition, 93 (3), 601-7 PMID: 21177796

Breast Milk of a Diabetic Mother

Over the course of the last century, human tissues as well as breast milk have accumulated a massive amount of polyunsaturated linoleic acid (omega 6) as discussed in THIS BLOG POST. This is due to a massive rise in the consumption of vegetable oils, peanut butter, and eating the fat of pigs and poultry (and eggs) fed mostly soy and corn (what cows are fed has little impact on the total linoleic acid content of their meat and milk).

As proposed in 180 Degree Metabolism, it’s hard not to suspect that these dietary changes have been responsible for many subsequent changes in our collective health. They have changed the composition of all of our cells and tissues in a multi-generational cumulative fashion, and this change in cellular composition has a lot of metabolic and inflammatory implications.

Okay I’ll stop sounding so freakin’ nerdy… These fats slow down your metabolism and cause you to produce extra inflammation – the commonality that modern scientists have found between countless seemingly unrelated health conditions.

Of course, one thing the modern world is faced with is this rising tide of hyperinsulinemia and rising blood sugars from our sucky glucose metabolism. Most blame this on carbohydrates despite utter failure of epidemiological evidence to back this theory up, and even more contradictions than what you see with the saturated fat kills hypothesis.

Anyway, Amy, a former La Leche League International leader, passed along an interesting study of the differences in the composition of breast milk in a diabetic mother. We know that children born to women with diabetes have a much higher risk of becoming obese and diabetic, and getting it younger than their parents did…

“Interestingly – and distressingly – we now see diabetes occurring ten to fifteen years earlier with each generation.”
-Virginia Valentine; Diabetes: The New Type 2

So what the heck would be the differences in a diabetic mama’s milk during this key priming period during a human’s development? Most mainstreamists would probably assume it’s higher in saturated fat and cholesterol and lower in “healthy fats,” like oleic acid found in olive oil and polyunsaturated fats found in nuts, seeds, and fish. In fact, in a mainstream book on type 2 diabetes, which the authors call “incurable,” and I would agree 100% when using the approach they call for – I found this fine chunk of dietary wisdumb…

“Avoid saturated fats such as butter, shortening, fats on meats, bacon, and tropical oils like coconut and palm oil. These same foods are also high in cholesterol and promote high levels of LDL cholesterol in the bloodstream.”
- Eisenstat, Stephanie A. and David M. Nathan. Every Woman’s Guide to Diabetes.

Actually, looking at the title of that book, one has to wonder if the book is a guide for having diabetes or a guide on how to get there. 


Well hey, don’t worry Sweet Steph and Diabetic Dave (Blooperheroes??). A diabetic mother has an innate wisdom to produce a diet for the young kid just like you advise. These were the differences between the diabetic mom’s breast milk and what is considered normal…

1) low cholesterol content, only one-fifth of normal milk;
2) decreased medium-chain [Saturated] fatty acids, suggesting impairment of fatty acid synthesis in the mammary gland;
3) increased oleic acid; and
4) high concentrations of polyunsaturated fatty acids, suggesting increased chain elongation.

Interesting, but sadly these wise guys still can’t manage to think outside the box, concluding…

“These results suggest that diabetes produces changes in lipid metabolism in the mammary gland that alter the composition of milk produced by the diabetic mother.”

I think it’s far more likely that an excess of polyunsaturated fats causes diabetes (and an alteration of milk composition), not diabetes causing excess of polyunsaturated fats!!! How would that even happen anyway?

For more on the accumulation of polyunsaturated fats, CLICK HERE

And here’s the study referred to in this post. Not a particularly significant study in terms of numbers or any kind of statistical relevance, but there are certainly no surprises in their findings.

Milk composition and volume during the onset of lactation in a diabetic mother. http://www.ncbi.nlm.nih.gov/pubmed/2596426

Indian Samosa Wraps

I created these beautiful and delicious Samosa Wraps tonight.  I had purchased Amy's Indian Samosa Wraps from the frozen section at Whole Foods and knew I could create these in my own kitchen.  I started with garlic, onion, potatoes and carrots.  After cooking for about 10 minutes, I added vegetable broth, peas, sun dried tomato, fresh jalapeno, salt, curry powder, ground ginger, coriander, cumin, cayenne pepper and lemon juice.  THE FLAVOR WAS SO DELICIOUS and only 4 grams of fat. Amy's Samosa Wraps were half the size of mine with more than double the fat.  I made my own whole wheat tortillas which were a blend between a tortilla and naan bread.  After making the tortillas, keep them wrapped so they stay soft until ready to use. 

Indian Samosa Wraps

Printable Recipe

Serves 4

2 cloves garlic (minced)

1/2 Tbsp.extra-virgin olive oil

3 medium potatoes (diced)

1/2 large onion (diced)

2 carrots (diced)

1 fresh jalapeno, seeded and diced

1 cup salt-free vegetable broth

1 cup frozen peas

1 sun-dried tomato (diced finely)

1 tsp. salt

1 Tbsp. curry powder

1 tsp. ground ginger

1/2 tsp. ground coriander

1/2 tsp. ground cumin

1/4 tsp. cayenne pepper

2 Tbsp. fresh lemon juice

homemade tortillas/naan bread

1.)  In a large skillet add 1/2 Tbsp. olive oil.  Add garlic and cook for 30 seconds stirring constantly.  Add potatoes, onion and carrots and cook for 10 minutes, stirring as needed.

2.)  Add 1 cup vegetable broth, sun-dried tomato, jalapeno, peas, salt, seasonings and lemon juice. 

3.)  Cover and let simmer until all liquid has been absorbed. Use a potato masher to mash your potato mixture somewhat.  Leave some chunks.

4.)  Divide mixture into 4 parts and put each part on each of the 4 tortillas.  Roll by bringing in the sides of the tortilla and rolling.  Warm if needed before serving. Slice in half and serve with spinach salad and orange slices. 

5.)  ENJOY!!

Wheat Tortillas

Makes 4

2 cups white whole wheat flour

2 tsp. aluminum free baking powder

1 tsp. salt

2 tsp. Earth Balance Butter

1 cup Coconut Milk (So Delicious 50 Calorie unsweetened)

1.) Mix together the flour, baking powder and salt.  Work in Earth Balance Butter with a hand pastry blender.

2.)  Slowly add warm coconut milk.  Stir until a loose, sticky ball is formed.

3.)  Knead for two minutes on a floured surface.  Dough should be firm and soft.  Place dough in a bowl and cover with a damp cloth for 30 minutes. This stage is very important.

4.)  After the dough has rested, divide into 4 equal parts.  Make each section into a ball and roll out to about a 10" - 12" circle.

5.)  Heat griddle to high.  Add first tortilla. Flip after a minute. Push tortilla down with spatula to produce air pockets.  Keep moving spatula around the tortilla to produce more air pockets.  Flip tortilla and continue with process until tortilla is lightly browned in a few areas of tortilla.  If desired you can brush tortilla lightly with Earth Balance Butter on one side.

6.)  Store tortillas under damp cloth until ready for use.

Brain Circuit Tied to Gambling Risk in Parkinson Disease Identified

Some of the drugs used to treat Parkinson disease (PD) increase the risk for pathological gambling.  This can have a significant economic adverse effect on some individuals.  I have previous posted on the use of amantadine in reducing pathological gambling in PD.  Although some medications may reduce the risk of pathological gambling, there is a need to further understand the mechanism of drug-related gambling behavior.

Cilia and colleagues from the University of Toronto as well as Italy recently published a study examining the neural network in a series of patients with PD and pathological gambling.   The research team used a brain imaging technique called SPECT.  SPECT is an earlier technology that measures brain anatomical blood flow.  In contrast to functional MRI, SPECT requires an intravenous injection of contrast agent.  In this study, the authors conducted a correlational analysis between regional cerebral blood flow and a measure of gambling severity from a psychometric instrument called the South Oaks Gambling Screen.   A series of subjects with PD  with pathological gambling were compared to a matched PD group without pathological gambling and a matched group without PD.   Using a complicated statistical analysis strategy called path analysis, they estimated effective brain connectivity (circuitry) associated with pathological gambling behavior.

High pathological gambling scores were associated with the reduced blood flow in the following brain regions (inpartial list):

• Right ventrolateral prefrontal cortex (VLPFC)
• Right anterior cingulate cortex (ACC)
• Right posterior cingulate cortex (PCC)
• Right medial frontopolar cortex (mPFC)
• Bilateral anterior insula
• Left striatum

The authors summarize why these specific regions and connections could affect the risk for development of pathological gambling behaviors.

Right VLPC: this brain region is involved with behavioral response inhibition, impulsivity and “risk-taking choices during decision making under conflict”.   Studies of damage to this region produces a “blunted reaction to aversive outcome and risk-taking behavior. 

ACC and striatum:  In healthy individuals, the authors note the ACC in a region involved in monitoring and processing negative outcomes.  The ACC regulates behavioral adjustments in scenarios where outcome predictability is low.  The ACC becomes activated in detecting errors after inhibition fails.   The striatum has previously been shown to be dysfunctional in problem gamblers without PD.  Dopamine (a neurotransmitter target of many PD drugs) is rich in the striatum and dopamine signaling mediates the “computation of reward prediction error and outcome expectation from future choices”.

The authors suggest that in PD gamblers, a disconnection develops between the ACC and striatum.  This may explain why they have difficulty with perserveration of behavior (continued gambling) despite continued monetary losses.

The authors note a weakness of their study is a reliance on correlational resting data.  A more powerful design would be to activate the brain regions involved in gambling with a task and study the anatomical and connectivity changes in those with PD associated with gambling and controls.  I suspect we will see such a study in the near future.

Image of Anterior Cingulate Cortex (ACC) Brain Region from 3D Brain Screen Shot Courtesy of Yates Photography.

Cilia R, Cho SS, van Eimeren T, Marotta G, Siri C, Ko JH, Pellecchia G, Pezzoli G, Antonini A, & Strafella AP (2011). Pathological gambling in patients with Parkinson's disease is associated with fronto-striatal disconnection: A path modeling analysis. Movement disorders : official journal of the Movement Disorder Society PMID: 21284039

Naps Boost Cognitive Performance in Seniors

Insomnia is a common complaint among elderly individuals. With aging, there is a pattern of decreased number of total sleep time and reduced time in deep sleep. Deep sleep is considered restorative sleep, an important component of feeling rested and alert the following day.


Sleep hygiene recommendations commonly warn against napping during the day time as it is felt to reduce the quantity and quality of sleep at night. However, many individuals report that napping during the day is helpful for them in getting sufficient sleep on a regular basis. Now there is some limited data that supports a role for regular napping for increasing total sleep time as well as some parameters of cognitive function.


Campbell and colleagues studied the effects of a month-long napping regimen in a series of individuals between the ages of 50 and 88 years of age. Key elements of the research design included:

• Inclusion criteria: age over 50 with self-reported good physical health, subjective insomnia complaints allowed but subjects had to score less than 5 on the Pittsburgh Sleep Quality Index and 2 or less on the sleep latency item from this scale, no regular sleeping medications, not taking psychotropic meds or other medications known to affect sleep, minor but not major medical problems, no periodic limb movements on baseline polysomnography
• Study variables/procedures: Sleep diaries and actigraphy at home 1 to 2 weeks before baseline laboratory examination, 3 consecutive nights and 2 days spent in sleep lab with polysomnography and neuropsychological testing including a test of logical reasoning, mathematical processing, letter memory search and reaction time test.
• Intervention: Randomization to either directed 45 minute nap or 2 hour nap, at least 5 times per week but recommended daily, to be completed in single setting before 6 pm to include daily sleep logs
• Outcome measures: Subjects returned for sleep lab evaluation for 2 nights at 2 and 4 weeks after randomization

The key elements of the outcome of the study:

• Napping did not change any of the night time sleep parameter: sleep onset latency, sleep efficiency or total nocturnal sleep time
• In 24 hour assessment of sleep both groups increased their total sleep time although as expected the long nap group had a longer total sleep time than the short nap group
• Neuropsychological performance improved in both groups at 2 and 4 weeks on three of the four neuropsychological measures (all but reaction time). The improvement was not statistically significant but the longer nap group tended to show greater improvement
• Adherence to recommended nap assignment: (9/11) in the short nap group met defined adherence while 5/10 in the long nap group met adherence—this difference was not significant

Although a small sample study, this research finding seems allay some concerns about a regular nap regimen for those over age 55 years of age. There does not appear to be evidence that napping impairs nocturnal sleep in duration or quality. The added sleep during the day with a nap in this study was accompanied by improvement in some elements of cognitive function. This improvement appeared to continue through 4 weeks and may not have reached its peak by that time. The authors note that none of the subjects were regular nappers before entering the study. 


So the take home message from the study is that for those 50 or older if you are taking a daily nap and feel it helps you, keep doing it. If you are not taking a daily nap and would like to consider adding one, it does not appear to be a risk for disrupting nocturnal sleep and you may get some cognitive boost from a daily napping regimen.


Photo of napping kittens courtesy of Wikepedia Commons author Tilman Piesk.


Campbell, S., Stanchina, M., Schlang, J., & Murphy, P. (2011). Effects of a Month-Long Napping Regimen in Older Individuals Journal of the American Geriatrics Society, 59 (2), 224-232 DOI: 10.1111/j.1532-5415.2010.03264.x

Female Masculinity, PCOS, Hirsutism

I’ve been fascinated with female masculinization, particularly facial hair growth or what is called hirsutism, ever since I heard about Diana Schwarzbein’s bout with a syndrome known as Stein Leventhal (Polycystic Ovarian Syndrome or PCOS basically). Okay, it started back before that, when Rebecca Romijn was the bearded lady in the movie Dirty Work, but that’s unrelated.



Recently this issue has been popping up again and again. For starters, last spring I had a female roommate who:

1) Was not menstruating
2) Had freakishly hairy arms that hadn't always been like that
3) Was super thin but stored fat in the lower back area only (male pattern fat storage)

Of course, this person was a misguided health fanatic that hadn’t always had these problems. Although I purposefully didn’t get into it with her knowing that there wasn’t the slightest chance I could transmit real knowledge into her gluten-free, dairy-free, vegetarian, low-calorie, alcoholic brain (I once heard her say that having a tooth abscess during a bout of the Master Cleanse was a sign of just how detoxifying the cleanse was, and that she was thinking of trying it again!), there is no doubt that she could have improved if not completely overcome her issue in a month by eating the food (ETF). It would have worked something like this:

1) ETF-ing raises thyroid output

2) Thyroid hormones flip the switch to decrease estrogen production and begin synthesizing more progesterone out of LDL

3) This decreases the amount of luteinizing hormone (LH) produced – (LH triggers the production of androgens – male hormones) while increasing free circulating progesterone which triggers a greater production of follicle stimulating hormone (FSH) – which in turn triggers ovulation and menstruation down the road

Voila – less androgen production, menstruation restored, and let’s hope it would increase some blood circulation to her brain as well.

This scenario was very similar to what you might see with someone with an eating disorder. Although some of the excess hair growth with anorexia is more like a peach fuzz, male-pattern hair on the chest and face as well as male-pattern baldness is very common.

But as any 180 junkie knows, there are many parallels between a person who is actually starving and a person who is overweight – and the key underlying commonality is a low metabolism/hypothyroidism.

So in those with insulin resistance with excess body fat you see the same kind of patterns emerging. Correspondence with a woman named Carla (not her real name) on Facebook recently may be of interest to you…

Carla noted that prior to her pregnancy she was always a warm 98.6 degree F kind of gal. Then she had a kid and suddenly noticed that her body temperature had plummeted to 97.2. Coinciding with this was of course, post-pregnancy weight gain of, I think she said 30-40 pounds without noticing much of a change in her normal diet and lifestyle patterns, and the development of thick, black facial hair. This is pretty classic PCOS/Stein-Leventhal kind of pathology. What fascinated me and is something that is NOT part of the known mainstream medical diagnostic portrait (anything of relevance rarely is) is that she noticed a coinciding drop in body temperature going along with all of this.

I can only assume that her body exhausted its capacity to produce progesterone during pregnancy, and when that faucet shut off she was left with a lot of metabolically-suppressive, androgen-stimulating, unopposed estrogen. But there are many other theories one could dream up, including perhaps her body’s unloading of her metabolically-stimulating short and medium chain saturated fats into breast milk while leaving nothing but linoleic acid (omega 6) in her body to stimulate estrogen.

This happens to a lot of women. Many women gain weight or can’t lose it after pregnancy, as well as enter into a mental state indicative of progesterone shortage (not totally unlike that experienced during PMS – presumably caused at least in part by insufficient progesterone levels at a time when they should be high). Anyway, she should get some relief if she can get her body temperature up. Not sure if she will pursue it or not. An excess of calories from coconut and dairy fat as well as carbohydrates would definitely help though.

Then we have ol’ Sheila – a 180 standby in the comments section both here and at the 180 Metabolism Blog. Sheila is a natural big testosterone producer for a woman, which led her to being coerced into female bodybuilding due to her hormonal profile for it. Bodybuilding led her to becoming very muscular, very lean, very cold, and very infertile. While she’s not out of the woods yet, she has at least brought her temperature up somewhat, had her period return after a very long vacation, and noticed an improvement in her overly-masculine voice and muscularity (if I’m not mistaken, I’m pretty sure she said that or something like it).

Last but not least for your interest, and to better help us all understand the hormonal and metabolic peculiarities of female masculinity, is a woman that I met recently. She contacted me after bringing her body temperature up 3.0 degrees F in 30 days following my overfeeding program. Prior to this she was a low-carb oriented Weston A. Price Foundation devotee and has been for years. She told me she has always been on the masculine side with excessive facial and chest hair.

And, not surprisingly, she has had her hormone levels tested and testosterone is off the charts, estrogen is moderate to high, and progesterone is about as low as can be. As a general rule I think it’s safe to say that testosterone is the default hormone for women to produce (they do so in the adrenal glands) when progesterone cannot be manufactured properly (due to stress, low metabolism typically). This high ratio of estrogen to progesterone by the way is very typical of a woman with breast cancer, and well, she’s definitely got breast cancer (bringing her body temperature up via RRARF didn’t help in the limited time she was able to try it by the way – and probably isn’t the best approach in late stage cancer despite its theoretical ability to increase cancer-obliterating cellular respiration).

Anyway, this female masculinity and PCOS stuff is interesting. If you are a woman and lean – having done a bunch of restricted diets, battled with eating disorders, engaged in hardcore competitive athletics – particularly endurance exercise, and stopped having your period and had some other complications develop… eat and eat some more.

On the topic of PCOS, which is more commonly something overweight women experience, beware of the approaches that just flat out tell you that PCOS is from “insulin resistance” and that you should cut out all carbohydrates. While this may seem like a miracle cure at first as you medicate your impaired glucose metabolism and temporarily bring your insulin levels down within normal ranges, eventually you will have to face the root cause of your impaired glucose metabolism instead of just avoiding it. Carbohydrate restriction, because it increases your exposure to stress hormones and “tends to shut down thyroid function” as Dr. Atkins put it, usually takes you to a dead end in a few years or less – with a myriad of new health problems like mood disorders, constipation, adrenal fatigue, mineral imbalances, and who knows what else.

The root cause, like most things, is probably a quintuple combination of excessive polyunsaturated fat accumulation in your tissues (which is estrogenic), excessive consumption of xenoestogens (toxic chemical pollutants) and phytoestrogens – soy being the worst offender, oral contraceptive use, excessive stress and inflammation, and repeated attempts at weight loss through any of the popular approaches ranging from doing lots of “cardio” to calorie restriction.

In other words, as usual, many of these health problems are caused by a “healthy low-calorie vegetarian diet with lots of healthy fats and healthy soy products and a healthy exercise program and healthy lifestyle” as we commonly define them in the 21st century. Eating and living in 180-Degree opposition to that should help tremendously. If all else fails, try natural, non-synthetic thyroid and progesterone supplementation.

If that fails too, join the circus. If you are anything like me, you’ll find hanging out with midgets a lot more fun than trying to eat a very low carbohydrate diet. And, you may find romance with an incredibly sexy, well-dressed man – just don’t be surprised when his fiancé shows up and throws egg salad sandwiches at you.

A Long Kiss
Big Top Pee-weeat MOVIECLIPS.com

Did the Red Fox Predate the Dog as Man's Best Friend?

Pets have longed played a role in human companionship.  Wild animals were primarily a source of food (and danger) in early human development.  Later in evolution,  animals began to serve a more complex role.  Domestication of a variety of animals served a more utilitarian role.  For example, domestication of horses allowed for extended travel, improved efficiency of hunting and provided a strategic advantage in battle.


The domestications of wild wolves has been felt to be one of the earliest examples of using animals for companionship and the development of a human/mammal pet relationship.  Now some recent archaelogical research suggests that the red fox may have predated the domesticated wolf as the original canine domesticated by humans.


Mather and colleagues present the case for the red fox predating domesticated wolves in a recent research summary in Plos One.  This research team includes members from the University of Cambridge in the UK as well as the University of Toronto.  Using findings from burial grounds in what is now northern Jordan, they lay out the evidence that the red fox predates the wolf as man's domesticated canine.


Seven human grave sites have been examined in the Uyun al-Hamman region between the Transjordanian Highlands and the Jordan valley.  The key elements from these findings include:

• Red fox skulls and bones are noted in several burial sites in proximity to human remains
• The proximity and manner of red fox bones suggest intentional placement rather than coincidence
• Some human bones were re-interred with movement and replacement of  red fox bones in the new grave
• This re-burial process suggests a personal relationship between the deceased human and a specific red fox--the transfer may have indicated an attempt that "the dead person would continue to have the fox with him or her in the afterlife"
• The pattern of remains are not consistent with some secondary process such as use the red fox as a pelt or as part of consumption of the animal
• The carbon dating data suggest this area and this burial site pre-dated by thousands of years the earliest known burial sites that include domesticated wolves
• Later grave sites show humans being buried with dogs supporting an emotional tie with social, ideological or symbolic significance

In summary, the research team feels these recent findings support an earlier "non-economic connections between people and animals".


I admit this post is outside my area of expertise.  However, we are becoming more aware of the potential importance of pet relationships in reducing loneliness, stress reduction and social psychology.  I do have to note that I took the photo of the red fox in this post in the winter of 2009-2010 in my back yard in Tulsa Oklahoma.  After a prolonged period of very low temperatures and frozen water sources, this red fox jumped a fence into my back yard and drank from our pool.  This research study suggests the red fox was one of man's earliest pets.  I'm happy to do whatever I can to aid this beautiful animal.


Photo of Red Fox Courtesy of Yates Photography


Maher, L., Stock, J., Finney, S., Heywood, J., Miracle, P., & Banning, E. (2011). A Unique Human-Fox Burial from a Pre-Natufian Cemetery in the Levant (Jordan) PLoS ONE, 6 (1) DOI: 10.1371/journal.pone.0015815

Autism: Social Lives of Young Adults

One of the problems with understanding the natural history of autism is the lack of well-designed outcome studies in the disorder.  Outcome studies tend to be expensive and grant agencies commonly do not fund studies longer than a few years. However, given the increased interest and funding in autism, I suspect there will be more research in this area.

An example of how outcome studies help in understanding the natural history of autism is a study published ahead of print by the Journal of Developmental and Behavioral Pediatrics.  Dr. Gregory Liptak and colleagues from SUNY Upstate present a four year follow up of 725 adolescents with autism.  The average age at intake was 15.4 years with average age at follow up 19.2 years.

The study examined some key global items in function and social interaction.  I summarize some of the factors related to three key areas of function (% with this variable):

Being employed (48%) or in postsecondary education: This two-option level of achievement was positively correlated with higher family socioeconomic status (above the poverty level), not needing prescription drugs to control symptoms, good general physical health and having a parent who was involved in the school.  Negative correlations for this level of achievement was associated with conversational difficulty, a history of being teased and lower IQ.

Obtaining a driver's license (4.5%):  Few adolescents or young adults in this sample had a drivers's license.  Again this achievement was associated with higher socioeconomic status, caucasian race, a two-parent household and parental involvement in school activities.  A negative correlation with obtaining a driver's license was higher number of required school services.

Getting together with friends at least once in last 12 months (44.6%):   A positive correlation was noted with communication ability and good general health status.  A weak negative association was noted with non-white race status and male gender.

The authors note that this group of young adults with autism showed persistent differences in academic achievement and  social behavior compared to age-matched adults without autism.  In the young adults with autism 83% were living with their parents and 75% never used instant messaging, a chat room or e-mail.

The authors noted that their study did not examine whether young adults with autism (or their families) wanted more social interaction.  We often assume the more social participation the better, but this may not be the same for all. 

Even prospective studies have some limitations on interpreting causal contributions to outcome.  However, this study supports several components to planning services for children with autism.  These include reducing effects of poverty, reducing teasing/bullying in the environment, encouraging parents to be active in the school setting, early social and speech therapy and management of physical and mental co-occurring conditions.  

Photo of Female Cardinal Courtesy of Yates Photography

Liptak GS, Kennedy JA, & Dosa NP (2011). Social Participation in a Nationally Representative Sample of Older Youth and Young Adults With Autism. Journal of developmental and behavioral pediatrics : JDBP PMID: 21285894

Brain Stimulation for Parkinson Disease: Expert Opinion

Parkinson disease is a chronic progressive disease with significant impairment and distress.  A host of pharmacological options are available. Unfortunately, drug treatment often is only partially successful in reducing symptoms and can produce problematic adverse events.  Deep brain stimulation (DBS) has emerged as a potential therapeutic option for those with severe Parkinson disease.  DBS involves a neurosurgical procedure that places an electrode or electrodes into the brain with a device to modulate an electric current.  The brain subthalamic nuclei has become the most common site for DBS electrode placement.

Many questions remain unanswered in DBS therapy for Parkinson disease.  A recent consensus conference assembled 49 experts in the use and care of patients receiving DBS therapy.  They have published their recommendations in a recent manuscript published in Archives of Neurology.  I will summarize some of their recommendations:

Surgical Selection:  Expert selection of candidates for DBS is viewed as the most important variable in getting a good DBS outcome.  Best candidates for DBS include those with the following features:

• Excellent response to the drug levodopa
• Younger age
• No or few axial motor symptoms that do not respond to levodopa
• Limited cognitive impairment
• Limited or well-controlled psychiatric disease

Surgical Complications: Surgical complications are not common but are not trivial and need to be taken into account when considering DBS surgery.  Complications can include intracranial hemorrhage (bleeding), stroke, infection, erosion of DBS leads, and death.  Advanced age and medical comorbidities appear to increase the risks for surgical complications but should not be absolute contraindications.  Surgical team experience is important and patients and their families should select centers with extensive experience with the procedure.  There is a need for a standardized system of reporting DBS complications to allow for comparison across treatment sites.

Parkinson Disease Outcome: If a patient has improvement in gait and speech with levodopa, they are more likely to have improvement in these domains with DBS.  Initial improvement in gait and speech with DBS may later fade as the disease progresses.  Some patients experience increase in depression after DBS and this may be related to the site of the electrodes.  Patients need to have depression, anxiety, apathy, psychosis and impulsivity levels assessed before surgery as these parameters may complicate outcome.  Improvement in some aspects of Parkinson disease has been demonstrated for up to 5 years.  Nevertheless, progression of disease commonly occurs in good DBS repsonders and DBS does not prevent the late stages of Parkinson disease including freezing of gait, postural instability and cognitive decline.

This expert consensus guideline will aid clinicians, patients and family members in considering DBS as a therapeutic option.  A patient resource for those with Parkinson disease considering DBS can be found here (DBS-STN.org-an affiliate of the Parkinson Alliance).

Figure of coronal section of brain showing subthalamic nuclei (STN in yellow)--common electrode placement site in DBS for Parkinson disease.  Figure courtesy of Creative Commons from Wikipedia, author Andrew Gillies.

Bronstein, J., Tagliati, M., Alterman, R., Lozano, A., Volkmann, J., Stefani, A., Horak, F., Okun, M., Foote, K., Krack, P., Pahwa, R., Henderson, J., Hariz, M., Bakay, R., Rezai, A., Marks, W., Moro, E., Vitek, J., Weaver, F., Gross, R., & DeLong, M. (2010). Deep Brain Stimulation for Parkinson Disease: An Expert Consensus and Review of Key Issues Archives of Neurology, 68 (2), 165-165 DOI: 10.1001/archneurol.2010.260

Cannabis Use and Psychosis (Part 2)

I reviewed a research study last fall examining a Dutch study of cannabis use and psychotic symptoms.  That post is linked here.  In summary, the study suggested cannabis probably does not produce psychotic symptoms in the majority of users.  However, if you have a family member with a psychotic disorder (suggesting you may have a genetic risk for psychosis) you may be more likely to experience psychotic symptoms (i.e. hallucinations/delusions) with cannabis use.  This risk may be increased with higher potency cannabis formulations.

Now two additional research publications weigh in on this issue.  Both were published in the February 2011 issue of Archives of General Psychiatry.  Both studies come from the Genetic Risk and Outcome of Psychosis (GROUP) study sample.

The first manuscript summarized the results of study using a sibling-control and cross-sibling comparison.  Eleven hundred twenty subjects with a psychotic disorder were compared to 1057 siblings and 590 controls. In summary the results of this study were:

• You were much more likely to report psychotic symptoms (both positive and negative psychotic symptoms) with cannabis use if you had a sibling with psychosis
• Siblings using cannabis resembled psychotic siblings in their ratings much more than siblings not using cannabis
• The statistical analysis of the relationship pointed to a familial risk increasing cannabis sensitivity, rather than familial risk increasing use of cannabis

So this finding in in line with the original study.  Families may resemble each other in the way they respond to cannabis.  Some families may be particularly more likely to have psychotic symptoms in the context of cannabis use.

The second study takes another step to try to explain this relationship.  Can candidate genes be identified that are linked to this cannabis-linked psychosis effect?  If so, do these genes make biological sense or do they seem to just likely be random associations.

The answers proposed by the GROUP investigators are intriguing.  

• Sixteen single nucleotide proteins (SNPs) showed significant interactions
• The AKT1 gene status (C/C genotype) increased risk of psychosis after cannabis use
• AKT1 gene status explained 19% of the variance of psychotic symptoms in siblings with recent cannabis use
• The AKT1 gene is regulated by endogenous cannabanoid signaling
• This signal is downstream from the dopamine D2 receptor--a receptor known to be involving in psychosis and the target of antipsychotic drugs

The authors note that their proposed mechanism explains two commonly clinical findings:

• antipsychotic drugs do not block the psychotic effect of THC in those that experience psychosis with the drug
• substance abusing patients with schizophrenia respond more poorly to antipsychotic treatment

The explanation would be the endocannabanoid AKT1 effect is downstream from the D2 receptor.  Blocking the D2 receptor would have limited effects downstream from the receptor.

These two studies add to support for a role for cannabis to be a potential risk factor for some forms of psychosis and schizophrenia.  The genetic and molecular correlations in this study a mutually supportive.  So the take home message seems to be the same--there just seems to be more support the message is research based.  Some individuals may have a genetic risk for psychotic symptoms related to cannabis use.  This is not a trivial risk.  If you have a sibling or other relative with psychosis, or if you experience psychotic symptoms with cannabis use, don't use cannabis.

Photo of Back Yard Blue Jay in Tulsa after Snowfall Courtesy of Yates Photography

., Kahn, R., Linszen, D., van Os, J., Wiersma, D., Bruggeman, R., Cahn, W., de Haan, L., Krabbendam, L., & Myin-Germeys, I. (2010). Evidence That Familial Liability for Psychosis Is Expressed as Differential Sensitivity to Cannabis: An Analysis of Patient-Sibling and Sibling-Control Pairs Archives of General Psychiatry DOI: 10.1001/archgenpsychiatry.2010.132

van Winkel, R., , ., Kahn, R., Linszen, D., van Os, J., Wiersma, D., Bruggeman, R., Cahn, W., de Haan, L., Krabbendam, L., & Myin-Germeys, I. (2010). Family-Based Analysis of Genetic Variation Underlying Psychosis-Inducing Effects of Cannabis: Sibling Analysis and Proband Follow-up Archives of General Psychiatry, 68 (2), 148-157 DOI: 10.1001/archgenpsychiatry.2010.152

Low-Fat Whole Wheat Molasses Cookies

I created these delicious low-fat whole wheat molasses cookies last week.  I absolutely loved their yummy

flavor and chewy texture. The also have a very nice nutritional analysis.  Per cookie: 2.1 g fat, 2.5 g fiber, 8.5 g sugar, 61 mg sodium, 1.5 g protein.

 

Low-Fat Whole Wheat Molasses Cookies

Printable Recipe

Makes 17 cookies

1 cup white whole wheat flour

1/2 cup rolled oats

1 tsp. non-aluminum baking powder

1/4 tsp. cinnamon

1/4 tsp. sea salt

2 Tbsp. organic blackstrap molasses

1/2 cup raw sugar

3 Tbsp. unsweetened almond milk (I made my own)

1 Tbsp. Earth Balance whipped butter

1 tsp. vanilla extract

1/4 cup chopped walnuts

1/4 cup raisins

Preheat oven to 350 F.  Combine dry ingredients in bowl.  Combine wet ingredients in small saucepan and warm until raw sugar is dissolved. Mix dry ingredients with wet, being careful not to over-mix the batter.

Drop by heaping tablespoon onto lightly greased baking sheet or use parchment paper.  Flatten each cookie with the bottom of a class.  To prevent sticking either flour bottom of glass or spray lightly with olive oil.

Bake cookies for 15 minutes.  Cool completely and store in airtight container to prevent cookies from hardening.

ENJOY!!

The New Conventional Wisdom

Years ago our teacher told us the story of the man who made canned tuna more popular than canned salmon. As I recall, this advertising guy had the account for some brand of canned tuna, which at the time was mostly being used as pet food. Most customers preferred canned salmon. What could he do to increase the public’s preference for this brand of tuna and thereby increase its sales? He came up with a simple slogan – “Guaranteed not to turn pink in the can.” Sales of canned tuna soon outpaced those of canned salmon. Was the man lying? No, his brand of tuna didn’t turn pink in the can. Neither did salmon, of course (or any other brand of tuna), but that’s beside the point.

This story makes two important points. First, it’s most likely a myth (see Snopes), but that hasn’t stopped it from being repeated endlessly as if it were true. The sincere repetition of false information as if it were true is common. Much of what we call “Conventional Wisdom” consists of just this sort of “knowledge.” Second, the practice of taking a it’s-true-but-so-what statement and making it the basis of an advertizing or public health campaign is alive and well.

Mark Sisson calls conventional wisdom his regular nemesis. It is the commonly accepted body of misinformation known by everyone, but unsupported by actual science. Everyone knows that lard and “other saturated fats” clog your arteries and cause heart disease. Reality TV shows (there’s an oxymoron) treat us to the spectacle of heavy folks being semi-starved and forcibly exercised into becoming lean, so everyone knows (including the “experts” that gave us the Dietary Guidelines for Americans, 2010) that eating less and exercising more is the key to attaining and maintaining a healthy weight. Everyone knows that “you are what you eat” and that the key to health is “all things in moderation.” The scientific literature, however, directly refutes each of these examples of common wisdom. So why, in the face of the current epidemic of obesity and chronic metabolic diseases, have the facts not impacted what everyone knows? It might have something to do with the hundreds of billions of dollars being made every year by the diet, fitness, health, medical, pharmaceutical, food processing, agriculture, regulatory, and public health industries.

Ancel Keys’ original hypothesis was that diets high in fat raised total serum cholesterol, which then produced atherosclerosis and heart disease. This is the infamous “Lipid Hypothesis” of heart disease. Within ten years, however, Keys modified his hypothesis to say that it was the saturated fat that produced the elevation in total serum cholesterol. He and his fellow lipophobes were then joined by members of the vegetarian-industrial complex, who were eager to seize on this message to promote their own interests.

There have always been people who, for a number of reasons (many of which are not justified - see Lierre Keith’s The Vegetarian Myth: Food, Justice, and Sustainability), don’t consume animal products. Since the primary sources of saturated fat in the American diet are animal products, Keys’ message supported the more evangelical vegetarians’ purposes quite well. The roots of the organic and sustainable agriculture movements are thoroughly entwined with the vegetarian belief system. Until recently, the terms “sustainable” and “organic” were synonymous with vegetarian. As these movements grew, their implicitly (and sometimes explicitly) anti animal products messages gained a wider audience. And then there’s the edible oil industry. They were quite happy to use the lipophobes’ message to promote their industrial products – corn oil, soybean oil, cotton seed oil, and derived products like margarine and Crisco – at the expense of their principle competition – natural products like lard, butter, and tallow. Their manufactured products were low in saturated fat and cholesterol. The natural animal products were not. This became the focus of their promotional campaigns. The statement of these differences was, of course, true. The health assertions, it turns out, were not. But they weren’t about to let the facts get in the way of a great sales strategy, so in addition to their own product marketing efforts they provided funding to various vegetarian-advocacy groups, disguised as “public health interest groups,” whose messages usually failed to mention either their benefactors or their principle beliefs. More and more heavily processed, plant-based “food” items are introduced every year, all of which tout their “healthfulness” because they’re low in the cholesterol and saturated fat that “has been linked with heart disease.” Yes, they’ve been “linked,” but what does that mean? It’s as truthful a statement as “won’t turn pink in the can!” Our current conventional wisdom is the result of this unhappy mix of ideology, dogma, and politics.

Unfortunately, it seems to me that we’re forming a new conventional wisdom within the low carb / paleo / primal / grass-finished and local food communities. It, too, is unsupported by the facts. For example, one concern of today’s consumer is the use, and the presumed presence in the meat, of artificial hormones. Poultry and pork are sold with claims of “no artificial hormones.” If you look carefully, you’ll see a very small footnote which states that it’s illegal to use artificial hormones to produce poultry and pork! The statement on the label is true, but so what? And oh, by the way. If you’re concerned about the potentially harmful effects of artificial hormones that might be in the meat you consume, don’t eat soy products. (See The Whole Soy Story: The Dark Side of America's Favorite Health Food by Kaayla T. Daniel.)

Another example: The other day I was reading a grass farming book by a well-known author who repeatedly stated that “chemical fertilizer burns out the soil organic matter.” Fertilizer can actually increase soil organic matter. The biggest factor in reducing soil organic matter is tillage. If you cultivate the soil, you’ll decrease that soil’s active organic matter fraction. There’s an association here, since most tillage agriculture involves the application of fertilizer, but association does not prove causation. If you keep the soil covered with long-term, perennial grass-clover pasture you will increase the soil’s organic matter content – regardless of how you fertilize it. In yet another example, the reporter in a news story examining grass finished beef stated that since the grass the cows were eating was “rich in healthy fat,” the meat was higher in omega 3 fatty acids than grain finished beef. Studies have shown that beef from grass finished cattle does have a lower omega 6 to omega 3 ratio, but the actual amount of omega 3 fatty acids may be about the same in both (only 13 milligrams more omega 3 per 3 ounce (85.5 gram) cooked portion). 1 Pasture herbage, by the way, is low-fat – usually less than 5% ether extract (“crude fat”). I must admit, it’s hard for me to read authors or listen to speakers who make these kinds of statements. If those who carry the message of low carb / paleo / primal way of life to the agricultural community repeat these examples of the new conventional wisdom, the danger is that our farmers and ranchers may not be able to listen to us, either.

When it comes to human health assertions for grass fed and finished animal products, I’m afraid the conversation is thoroughly tainted by the old conventional wisdom. Gary Taubes has emphasized the critical role that brutal criticism plays in a healthy science. New ideas are subjected to harsh critique from one’s peers. Without this type of internal review, false ideas can contaminate the science – not just the discipline they come from, but many others as well. The realm of human nutrition hasn’t had this kind of healthy critique for more than 50 years, and the contagion of its flawed reasoning and theories has spread widely. Most research papers regarding grass based animal products contain statements that summarize either the lipid hypothesis or the calories-in/calories-out hypothesis, or both. The other day I received a newsletter from a local grass finished meat supplier which, naturally enough, listed several statements meant to describe the benefits of grass finished over grain finished beef. Here are their points, along with my comments:

"Grass fed beef has about the same amount of fat as skinless chicken and wild game, adding beef to the list of food that actually could lower your LDL cholesterol."

Grass Finished Beef, NOT Low Fat!

That grass-finished beef is low fat may be true (although there are variations due to breed, etc., that make this a less-than universally true statement), but that’s only a good thing if you believe the lipid hypothesis. The truth is that the fatty acids in beef, either grass or grain finished, will actually improve your blood lipid profile! In general beef fat is 50 percent saturated fatty acids (one third of which is stearic fatty acid, which our bodies convert to oleic acid 2 – the primary fatty acid in olive oil), 42 percent monounsaturated fatty acids (90% of which is oleic acid), and 4 percent polyunsaturated fatty acids. 3 The science has shown that, in fact, eating beef tallow instead of carbohydrates would improve your blood lipid profile and lower your Coronary Heart Disease risk! [58 percent of the fat in beef tallow will improve your LDL:HDL cholesterol ratio. The remaining 42 percent will raise LDL cholesterol, but will also raise HDL cholesterol and will have an insignificant effect on the total cholesterol:HDL ratio.] 4

What's the "Heart-Healthy" Portion of this Meal?

"Assuming you eat a typical amount of beef, in a year, by switching to Grass fed beef you could save 18,000 calories a year. Which means if you change nothing else in your diet you could lose 6 pounds a year just by changing where your beef comes from."

This is an attempt to apply the failed calories-in vs. calories-out theory of obesity. For a detailed discussion of why this theory is not correct, please see Gary Taubes’ blog post The Inanity of Overeating and his newest book, Why We Get Fat, And What to Do About It.

"4o% of American’s don’t get enough Omega-3 fatty acids, the “good fat”. Not only are they important to the brain, they also play a role in every cell and system in the body. By keeping your brain healthy you are less likely to suffer from depression, schizophrenia, attention deficit disorder and Alzheimer’s. “Good fats” are linked to lowering blood pressure, reducing heart attacks, fighting depression and reducing cancer."

The phrase “good fats” belies the lingering taint of lipophobia. Dietary fat, saturated or not, is not a cause of obesity, heart disease or any other chronic “disease of civilization.” 5 (see Grass and Cancer). Refined carbohydrates, starches, and sugars are the most likely dietary causes of cancer, Alzheimer’s disease, and the other chronic diseases of civilization. 6 Diets low in carbohydrate are necessarily high in fat, typically animal fat. So, all animal fats have been “linked” to these improvements in health. In addition, beef, grass-finished or grain-finished, is a relatively poor source of omega 3 fatty acids when compared to oily fish, like wild-caught salmon.

"Omega-6 fatty acids are vital for human health. The bad news is; a diet too rich in these Omega 6’s had been linked to obesity, diabetes, immune system disorders and cancer! In order to function well our bodies require a balance between Omega-3 & Omega-6 fatty acids. Ideally 1:1 is the best ratio, grass fed beef is 2:1, while feed lot (grain fed, store bought) beef has a ratio of over 20:1. Huge difference!"

Yes, there is a huge difference between 1:1 and 20:1. That’s a true statement. But as shown by Duckett, et al., 7 the omega 6 to omega 3 ratio in grain-finished beef can be as low as 4:1. I’ve seen the 20:1 figure cited as the ratio of the typical American diet as a whole, so it appears they got these figures confused. As I’ve discussed previously (What’s the Limiting Factor?), just how important would this difference be if dietary carbohydrates are not restricted? How likely would someone be to realize any benefit?

"5 times more CLA is found in meat raised on grass. CLA can help prevent cancer and reduce cancer-cell growth."

As stated previously, the most likely dietary cause of cancer is refined carbohydrates. Restricting those while eating beef, regardless of how it was finished, is quite likely to prevent cancer (see Grass and Cancer). Coupled with appropriate supplementation of vitamin D, the impact is likely to be far in excess of that suggested by the conjugated linoleic acid (CLA) research.

"The National Cattlemen's Beef Association has noted that grass-fed beef has eight times more vitamin B12, six times more zinc and two and a half times more iron than skinless chicken breast."

This is true of beef, regardless of how it’s finished! 8

Until the flawed and failed lipid hypothesis of heart disease and the calories-in/calories-out hypothesis of obesity are fully discarded, we won’t make meaningful progress against the epidemic of chronic illnesses we face today. That awareness, coupled with the acceptance of the fundamental requirement for animal products for optimal human health, will permit us to have a meaningful discussion about the health benefits of grass fed and finished animal products. Until then, we must guard against creating a new conventional wisdom.

References

1 S. K. Duckett, J. P. S. Neel, J. P. Fontenot, and W. M. Clapham. 2009. “Effects of winter stocker growth rate and finishing system on: III. Tissue proximate, fatty acid, vitamin, and cholesterol content.” Journal of Animal Science 2009.87:2961-2970.

2 Grundy, S. M. 1994. “Influence of Stearic Acid on Cholesterol Metabolism Relative to Other Long-Chain Fatty Acids.” American Journal of Clinical Nutrition. Dec.; 60(6 suppl.):986S-90S

3 USDA. 2010. Composition of Foods Raw, Processed, Prepared. USDA National Nutrient Database for Standard Reference. Release 23 http://www.nal.usda.gov/fnic/foodcomp/search/

4 Taubes, Gary. 2008. Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease. Anchor Books. New York, NY. pp 168-169

5 Ibid p 454

6 Ibid

7 S. K. Duckett, J. P. S. Neel, J. P. Fontenot, and W. M. Clapham. 2009. “Effects of winter stocker growth rate and finishing system on: III. Tissue proximate, fatty acid, vitamin, and cholesterol content.” Journal of Animal Science 2009.87:2961-2970.

8 USDA. 2010. Composition of Foods Raw, Processed, Prepared. USDA National Nutrient Database for Standard Reference. Release 23 http://www.nal.usda.gov/fnic/foodcomp/search/ [A comparison of “Beef, round, outside round, bottom round, steak, separable lean and fat, trimmed to 0” fat, all grades, cooked, grilled” with “Chicken, broilers or fryers, breast, meat only, cooked, roasted.”]