Tag Archives: mild cognitive impairment

January 17, 2013 · 4:46 AM

Sugar and Carbohydrates Linked to Impaired Brain Function in Elderly

 

Note the sugar cubes

Note the sugar cubes

The Mayo Clinic recently reported that diets high in carbohydrates and sugar increase the odds of developing cognitive impairment in the elderly years.

Mild cognitive impairment is usually a precursor to dementia.  Many authorities think dementia develops more often in people with diabetes, although some studies refute the linkage.

Mayo investigators followed 940 patients with normal baseline cognitive functioning over the course of four years. Diet was assessed via questionnaire. Study participants were ages 70 to 89. As the years passed, 200 of them developed mild cognitive impairment.

Compared with those eating at the lowest level of carbohydrate consumption, those eating at the highest levels were almost twice as likely to go to develop mild cognitive impairment.

The scientists note that those eating lower on the carbohydrate continuum were eating more fats and proteins.  Whether the Low-Carb Mediterranean Diet prevents cognitive impairments remains to be seen.

Steve Parker, M.D.

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November 29, 2012 · 5:40 AM

Low-Carb Research Update

“What about that recent study in American Journal of Clinical Nutrition…?”

As much as possible, I base my nutrition and medical recommendations on science-based research published in the medical literature.  Medical textbooks can be very helpful, but they aren’t as up-to-date as the medical journals.

In the early 2000s, a flurry of research reports demonstrated that very-low-carb eating (as in Dr. Atkins New Diet Revolution) was safe and effective for short-term weight management and control of diabetes.  I was still concerned back then about the long-term safety of the high fat content of Atkins.  But 80 hours of literature review in 2009 allowed me to embrace low-carbohydrate eating as a logical and viable option for many of my patients.  The evidence convinced me that the high fat content (saturated or otherwise) of many low-carb diets was little to worry about over the long run.

By the way, have you noticed some of the celebrities jumping on the low-carb weight-management bandwagon lately?  Sharon Osbourne, Drew Carey, and Alec Baldwin, to name a few.

My primary nutrition interests are low-carb eating, the Mediterranean diet, and the paleo diet.  I’m careful to stay up-to-date with the pertinent scientific research.  I’d like to share with you some of the pertinent research findings of the last few years.

Low-Carb Diets

  • Low-carb diets reduce weight, reduce blood pressure, lower triglyceride levels (a healthy move), and raise HDL cholesterol (another good trend).  These improvements should help reduce your risk of heart disease.  (In the journal Obesity Reviews, 2012.)
  • Dietary fat, including saturated fat, is not a cause of vascular disease such as heart attacks and atherosclerosis (hardening of the arteries).  (Multiple research reports.)
  • If you’re overweight and replace two sugary drinks a day with diet soda or water, you’ll lose about four pounds over the next six months.  (American Journal of Clinical Nutrition, 2012.)
  • United States residents obtain 40% of total calories from grains and added sugars.  Most developed countries are similar.  Dr. Stephan Guyenet notes that U.S. sugar consumption increased steadily “…from 6.3 pounds [2.9 kg] per person per year in 1822 to 107.7 pounds [50 kg] per person in 1999.  Wrap your brain around this: in 1822 we ate the amount of added sugar in one 12-ounce can of soda every five days, while today we eat that much sugar every seven hours.”
  • A very-low-carb diet improves the memory of those with age-related mild cognitive impairment. Mild cognitive impairment is a precursor to dementia.  (University of Cincinnati, 2012.)
  • High-carbohydrate and sugar-rich diets greatly raise the risk of mild cognitive impairment in the elderly. (Mayo Clinic study published in the Journal of Alzheimers’ Disease, 2012.)
  • Compared to obese low-fat dieters, low-carb dieters lose twice as much fat weight.  (University of Cincinnati, 2011.)
  • Diets low in sugar and refined starches are linked to lower risk of age-related macular degeneration in women.  Macular degeneration is a major cause of blindness.  (University of Wisconsin, 2011.)
  • A ketogenic (very-low-carb) Mediterranean diet cures metabolic syndrome (Journal of Medicinal Food, 2011.)
  • For type 2 diabetics, replacing a daily muffin (high-carb) with two ounces (60 g) of nuts (low-carb) improves blood sugar control and reduces LDL cholesterol (the “bad” cholesterol). (Diabetes Care, 2011.)
  • For those afflicted with fatty liver, a low-carb diet beats a low-fat diet for management. (American Journal of Clinical Nutrition, 2011.)
  • For weight loss, the American Diabetes Association has endorsed low-carb (under 130 g/day) and Mediterranean diets, for use up to two years. (Diabetes Care, 2011.)
  • High-carbohydrate eating doubles the risk of heart disease (coronary artery disease) in women.  (Archives of Internal Medicine, 2010.)
  • One criticism of low-carb diets is that they may be high in protein, which in turn may cause bone thinning (osteoporosis).  A 2010 study shows this is not a problem, at least in women.  Men were not studied.  (American Journal of Clinical Nutrition.)
  • High-carbohydrate eating increases the risk of developing type 2 diabetes (American Journal of Clinical Nutrition, 2010.)
  • Obesity in U.S. children tripled from 1980 to 2000, rising to 17% of all children.  A low-carb, high-protein diet is safe and effective for obese adolescents.  (American Journal of Clinical Nutrition, 2010.)

Mediterranean Diet

The traditional Mediterranean diet is well established as a healthy way of eating despite being relatively high in carbohydrate: 50 to 60% of total calories.  It’s known to prolong life span while reducing rates of heart disease, cancer, strokes, diabetes, and dementia.  The Mediterranean diet is rich in fresh fruits, vegetables, nuts and seeds, olive oil, whole grain bread, fish, and judicious amounts of wine, while incorporating relatively little meat.  It deserves your serious consideration.  I keep abreast of the latest scientific literature on this diet.

  • Olive oil is linked to longer life span and reduced heart disease.  (American Journal of Clinical Nutrition, 2012.)
  • Olive oil is associated with reduced stroke risk.  (Neurology, 2012).
  • The Mediterranean diet reduces risk of sudden cardiac death in women.  (Journal of the American Medical Association, 2011.)
  • The Mediterranean diet is linked to fewer strokes visible by MRI scanning.  (Annals of Neurology, 2011.)
  • It reduces the symptoms of asthma in children.  (Journal of the American Dietetic Association, 2011.)
  • Compared to low-fat eating, it reduces the incidence of type 2 diabetes by 50% in middle-aged and older folks.  (Diabetes Care, 2010.)
  •  A review of all available well-designed studies on the Mediterranean diet confirms that it reduces risk of death, decreases heart disease, and reduces rates of cancer, dementia, Parkinson’s disease, stroke, and mild cognitive impairment.  (American Journal of Clinical Nutrition, 2010.)
  • It reduces the risk of breast cancer.  (American Journal of Clinical Nutrition, 2010.)
  • The Mediterranean diet reduces Alzheimer’s disease.   (New York residents, Archives of Neurology, 2010).
  • It slows the rate of age-related mental decline.  (Chicago residents, American Journal of Clinical Nutrition, 2010.)
  • In patients already diagnosed with heart disease, the Mediterranean diet prevents future heart-related events and preserves heart function.  (American Journal of Clinical Nutrition, 2010.)

Clearly, low-carb and Mediterranean-style eating have much to recommend them.  Low-carb eating is particularly useful for weight loss and management, and control of diabetes, prediabetes, and metabolic syndrome.  Long-term health effects of low-carb eating are less well established.  That’s where the Mediterranean diet shines.  That’s why I ask many of my patients to combine both approaches: low-carb and Mediterranean.  Note that several components of the Mediterranean diet are inherently low-carb: olive oil, nuts and seeds, fish, some wines, and many fruits and vegetables.  These items easily fit into a low-carb lifestyle and may yield the long-term health benefits of the Mediterranean diet.  If you’re interested, I’ve posted on the Internet a Low-Carb Mediterranean Diet that will get you started.

Steve Parker, M.D.

Disclaimer:  All matters regarding your health require supervision by a personal physician or other appropriate health professional familiar with your current health status.  Always consult your personal physician before making any dietary or exercise changes.

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July 24, 2011 · 2:00 AM

Research Round-Up

 

I have a stack of scientific articles I’ve been meaning to review in depth and blog about.  But I have to finally admit I don’t have the time.  Here they are.  Click through for details.

  1. Long-term calorie restriction in humans appears highly effective in reducing atherosclerosis risk factors (lab tests) and actual carotid artery atherosclerosis. Only 18 study subjects, however.
  2. A very-low-carbohydrate diet improved memory in older adults with mild cognitive impairment over six weeks.  Twenty-three subjects were randomized to either high-carb or very-low-carbohydrate diet.  The low-carbers improved verbal memory performance, lost weight, reduced fasting blood sugar and fasting insulin levels.  Ketone levels were positively correlated with memory performance.
  3. A high-fat diet impairs cognitive function and heart energy metabolism in young men.  Sixteen test subjects.  Crossover study design with a five-day high-fat diet deriving 75% of energy from fat, compared to a low-fat diet deriving 23% of energy from fat.  High-fat diet led to impaired attention, speed, and mood.  I’m sure low-carb bloggers have been all over this.  At first blush, it appears they were testing during “induction flu” phase of very-low-carb eating, between days 2 to 7 of a new ketogenic diet.  It takes several weeks to adapt metabolism to running almost entirely on fat rather than standard carbohydrates.  Suspect results would have been different if given time to adapt.
  4. Weight-loss with the laparoscopic gastric banding procedure has poor long-term outcome, according to Belgian surgeons reporting on 82 patients.  Four in 10 patients had major complications.  Nearly half of the 82 patients needed to have the bands removed, and six of every 10 required some kind of re-operation.
  5. Trust me, you DON’T want age-related macular degeneration.  Women, reduce your risk of ARMD with a healthy lifestyle, including regular exercise, avoidance of smoking,  and by eating abundant plant foods (vegetables [including orange and dark leafy green ones], fruits, and whole grains) and limit foods high in fat, refined starches, sugar, alcohol, and oils.  At least according to these researchers. 
  6. Leafy green vegetables and olive oil are linked to reduced heart disease (CHD) in Italian women.  Fruit consumption had no effect.  This is from a subset of the huge EPIC study, following 30,000 women over almost eight years.
  7. The Mediterranean diet protects against metabolic syndrome, reducing risk by about a third according to a huge meta-analysis from Greek and Italian investigators.  It works best in Mediterranean countries. 
  8. The Mediterranean diet was linked to slower rates of cognitive decline in Chicago residents over the course of almost eight years.  The comparison diet was the Healthy Eating Index-2005.  Of the 3,800 participants, about two-thirds were black.  A Manhattan population showed lower risk of dementia when eating Mediterranean-style.

There ya’ go.  This is better than letting the articles just sit in my briefcase for months on end, eventually to be thrown out.

Steve Parker, M.D.

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March 25, 2011 · 2:05 AM

Vitamins Slow Rate of Brain Shrinkage in Elderly

A cocktail of three common vitamins slowed the rate of brain shrinkage over two years  in elderly patients with mild cognitive impairment, according to researchers at the University of Oxford.  Less brain shrinkage should translate to better brain functioning.  People with diabetes need to know about this since diabetes is associated  with age-related cognitive impairment and dementia.  The dementia connection is debatable.

As a hospitalist, I see 10 or 20 brain scans every week.  A healthy 40-year-old brain nicely fills out the allotted space in the skull.  Most 70-year-old brains have an obvious degree of shrinkage.  Those with the most shrinkage typically have worse mental functioning, often diagnosed clinically as dementia, or its precursor, mild cognitive impairment (MCI).

The medical term for brain shrinkage is brain atrophy.  It reflects loss of brain cells or decrease in brain cell size.  I see A LOT of atrophied brains and impaired mental functioning—aka diminished cognition—in the elderly. 

Not everybody with atrophy has mental impairment; healthy brains slowly atrophy with age.  Alzheimer’s disease patients atrophy quickly; MCI patients atrophy at an intermediate rate.  MCI patients converting over the years to Alzheimer’s show a faster rate of atrophy.

Mild cognitive impairment affects 14 to 18% of those over age 70 (five million in the U.S.).  Half of these convert to Alzheimer’s disease or another dementia within five years.  We desperately need a way to prevent or slow that conversion.

That’s why I was excited to see a research report in which brain atrophy was slowed with three simple daily vitamins: folic acid 800 mcg, B12 500 mcg, and B6 20 mg.  (One Centrum vitamin, by comparison, provides folic acid 400 mcg, B12 6 mcg, and B6 2 mg).  The investigators will report later on whether the vitamins helped prevent mental decline.

These three vitamins are involved in homocysteine metabolism; they decrease blood levels of homocysteine.  Read elsewhere if you want the boring details. 

Methodology

Oxford area participants were at least 70 years of age and had mild cognitive impairment but not dementia.  Blood homocysteine levels were drawn periodically.  Participants were randomized to take either placebo (83 subjects) or the daily vitamins (85 subjects) for two years.  MRI scans were done periodically to determine brain volume.  Tests of mental functioning were done periodically.  More subjects were in the study at the outset but some dropped out and others didn’t have technically adequate MRI scans.

Results

After adjustment for age, the annual rate of brain atrophy was 30% less in the vitamin group compared to placebo.

For the placebo group, the rate of brain atrophy was clearly related to baseline homocysteine levels: higher homocysteine, faster atrophy.

Although the study was not powered to detect an effect of treatment on cognition (findings to be reported separately), in a post hoc analysis, we noted that final cognitive test scores were correlated to the rate of atrophy.

Atrophy appears to be a major determinant of cognitive decline in this population.

There were no significant safety issues and no differences in adverse events between the groups.

The vitamin group lowered homocysteine levels by 32% compared to placebo.

Reduction in brain shrinkage rate was best in those with a higher baseline homocysteine level (over 13 micromol/L); those with the lowest baseline levels (<9.5 micromol/L) showed no effect of vitamin therapy.  [In the U.S., 13% of those over 60 have concentrations over 13 micromol/L, whereas the median is 10 micromol/L.]

Comments

Although this is small study, I’m excited about the future clinical implications.  The results need to be replicated.  I can’t wait to hear from this group regarding the details of mental functioning tests.  If preservation of brain function or other practical benefits don’t accompany a slower rate of atrophy , it’s no use taking the vitamins.

A 2008 study found no clinical benefit with a similar vitamin mix in Alzheimer’s patients with mild to moderate disease.  In other words, the rate of mental decline was no different than the placebo group.  Average homocysteine level was 9.16 micromole/L and fell by 30% during the 18-month-long study.  Even those with the highest homocysteine levels showed no benefit.  Perhaps B vitamins need to be started much earlier in the disease process to be effective.

The time may come where we screen all 60-year-olds for above-average homocysteine levels, starting them on the vitamin cocktail.

One caveat, however.  Ten years ago doctors were quite excited about preventing heart disease events (e.g., heart attacks, cardiac deaths) and strokes in people with high homocysteine levels.  We knew that high levels were associated with cardiac events and strokes, and we knew the B vitamins would lower the blood levels.  We learned a couple years ago that B vitamin therapy actually didn’t help heart patients or those at high risk for heart disease.  Nor do the vitamins prevent strokes.  [If you’re a heart patient still taking Foltx, ask your cardiologist if it’s OK to stop it now.]

Steve Parker, M.D.

References: 

Smith, David, et al.  Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: A randomized controlled trial.  PLoS ONE 5(9): e1244.  doi: 10.1371/journal.pone.0012244  [published September 8, 2010]

Aisen, P.S., et al.  High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: A randomized controlled trial.  Journal of the American Medical Association, 300 (2008): 1,774-1,783.

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September 21, 2010 · 2:00 AM

Myth Busted: Alzheimer Dementia NOT Caused By Diabetes

Contrary to popular belief among the experts, type 2 diabetes is not one of the causes of Alzeimer dementia.  They may indeed be associated with each other, but that’s not causation. 

Brain CT scan

An oft-repeated theory from Gary Taubes 2007 masterpiece, Good Calories, Bad Calories, is that many of the chronic diseases of modern civilization, including Alzheimer disease, are caused by abnormal blood sugar and insulin metabolism.  Especially high insulin levels induced by a diet rich in refined carbohydrates.  If that’s the case, you’d expect to see a high prevalence of Alzheimer disease in older type 2 diabetics. 

Dr. Emily Deans (psychiatrist) has been considering this issue recently at her Evolutionary Psychiatry blog.

The brains of Alzheimer patients, under a microscope, are characterized by many senile plaques (aka neuritic plaques) and neurofibrillary tangles.  That’s the gold standard for diagnosis.  Nevertheless, brain biopsies are rarely done to diagnose Alzheimer disease in living patients, and even autopsies after death are rare.  The diagnosis usually is clinical, based on ruling out other illnesses, etc.

Nearly all the studies associating diabetes with Alzheimers disease (and other dementias) are observational or epidimiologic. [The exception is the Honolulu-Asia Aging Study.]  Establishing an association is helpful in generating theories, but establishing causation is the goal.  At least five studies confirm an association.

Neurology this year reported findings of Japanese researchers who examined the brains of 135 people who died between 1998 and 2003.  They lived in Hisayama, a town with an incredibly high autopsy rate of 74%.  These people before death had undergone an oral glucose tolerance test.  Their insulin resistance was calculated on the basis of fasting glucose and fasting insulin (HOMA-IR).  None of them showed signs of dementia at the time of study enrollment in 1988.

What Did They Find?

Twenty-one of the 135 subjects developed Alzheimer-type dementia.  The investigators don’t say if the diagnosis was based on the brain examination, or just a clinical diagnosis without a brain biopsy.  How this got beyond the article reviewers is beyond me.  [If I’m missing something, let me know in the comments section below.]  It must be a clinical diagnosis because if you don’t act demented, it doesn’t matter how many senile plaques and neurofibrillary tangles you have in your brain. 

ResearchBlogging.orgSenile plaques, but not neurofibrillary tangles, were more common  in those with higher levels of blood sugar (as measured two hours after the 75 g oral glucose dose), higher fasting insulin, and higher insulin resistance.  People with the APOE epsilon-4 gene were at even higher risk for developing senile plaques.

The researchers did not report whether the subjects in this study had been previously during life with diabetes or not.  One can only hope those data will be published in another paper.  Why make us wait? 

Average fasting glucose of all subjects was 106 mg/dl (5.9 mmol/l); average two-hour glucose after the oral glucose load was 149 mg/dl (8.3 mmol/l).  By American Association of Clinical Endocrinologists criteria, these are prediabetic levels.  Mysteriously, the authors fail to mention or discuss this.  [I don’t know if AACE criteria apply to Japanese.]  Some of these Japanese subjects probably had diabetes, some had prediabetes, others had normal glucose and insulin metabolism.

As with all good research papers, the authors compare their findings with similar published studies.  They found one autopsy study that tended to agree with their findings (Honolulu) and three others that don’t (see references below).  In fact, one of the three indicated that diabetes seems to protect against the abnormal brain tissue characteristic of Alzheimer disease.

Botton Line

Type 2 diabetes doesn’t seem to be a cause of Alzheimer disease, if autopsy findings and clinical features are the diagnostic criteria for the disease. 

If we assume that type 2 diabetics have higher than normal blood sugar levels and higher insulin levels for several years, then hyperglycemia and hyperinsulinemia don’t cause or contribute to Alzheimer dementia.  Myth busted.  [I hope that’s not copyrighted by the “Myth Busters” TV show.]

Type 2 diabetes is, however, linked with impaired cognitive performance, at least according to many of the scientific articles I read in preparation for this post.  So type 2 diabetics aren’t in the clear yet.  It’s entirely possible that high blood sugar and /or insulin levels cause or contribute to that.  [Any volunteers to do the literature review?  Best search term may be “mild cognitive impairment.”]

Type 2 diabetes is associated with Alzheimer disease, but we have no proof that diabetes is a cause of Alzheimers.  Nor do we have evidence that high blood sugar and insulin levels cause Alzheimer disease. 

Alzheimer disease is a major scourge on our society.  I’d love to think that carbohydrate-restricted eating would help keep blood sugar and insulin levels lower and thereby lessen the devastation of the disease.  Maybe it does, but I’d like to see more convincing evidence.  It’ll be years before we have a definitive answer. 

Steve Parker, M.D.

References:
Matsuzaki T, Sasaki K, Tanizaki Y, Hata J, Fujimi K, Matsui Y, Sekita A, Suzuki SO, Kanba S, Kiyohara Y, & Iwaki T (2010). Insulin resistance is associated with the pathology of Alzheimer disease: the Hisayama study. Neurology, 75 (9), 764-70 PMID: 20739649

Heitner, J.,  et al. “Diabetics do not have increased Alzheimer-type pathology compared with age-matched control subjects: a retrospective postmortem immunocytochemical and histofluorescent study.” Neurology, 49 (1997): 1306-1311.  Autopsy study, No. of subjects not in abstract. They looked for senile plaques and neurofibrillary tangles, etc. The title says it all.

Beeri,  M.S., et al. “Type 2 diabetes is NEGATIVELY [emphasis added] associated with Alzheimer’s disease neuropathology.” J. Gerontol A. Biol Sci. Med. Sci. 60 (2005): 471-475.  385 autopsies. The title again says it all.

Arvanitakis, Z., et al. “Diabetes is related to cerebral infarction but NOT [emphasis added] to Alzheimers disease pathology in older persons.”  Neurology, 67 (2006): 1960-1965. Autopsy study of 233 Catholic clergy, about 50:50 women:men.

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