Category Archives: Dementia

Science magazine has been investigating this for six months. This is disturbing, to say the least.

For several decades, a leading theory on the “cause” of Alzheimer disease is that a toxic protein called beta amyloid builds up in certain parts of the brain, impairing function. If that’s true, the next questions are 1) why does the protein accumulate, and 2) what can be done to prevent it.

From ABC News:

Allegations that part of a key 2006 study of Alzheimer’s disease may have been fabricated have rocked the research community, calling into question the validity of the study’s influential results.

Science magazine said Thursday that it uncovered evidence that images in the much-cited study, published 16 years ago in the journal Nature, may have been doctored.

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More than $1 billion of government funding, through the National Institutes of Health, has been directed to amyloid-related Alzheimer’s research. While the investigation suggests that studies of Aβ*56 should be opened up to new scrutiny, experts said the entire theory shouldn’t be discredited.

Steve Parker, M.D.

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I’m tempted to get my blood level of 25-hydroxyvitamin D checked.

Dr. John Campbell is “totally convinced” that high-dose vitamin D supplementation would prevent many cases of dementia, particularly Alzheimer dementia, which is 75% of all dementia cases. He takes 4,000 IU of vitamin D/day plus 100 mcg of vitamin K2. Unclear to me if that’s year-round or only in fall and winter. I assume it’s oral vitamin D3 (there are several types of vitamin D). Dr. Campbell didn’t say why he takes the K2. Click for a brief review of K2. In contrast to his vitamin D dose of 4,000 IU/day, U.K. health authorities recommend a tenth of that — 400 IU — in autumn and winter.

Several observational studies link higher risk of dementia with blood levels of vitamin D that are deficient or insufficient. Blood levels of 25-hydroxy-vitamin D under 25 mg/ml are particularly linked to dementia. Dr. Campbell admits that it’s difficult to prove that adequate vitamin D supplementation would prevent Alzheimer dementia.

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  Steve Parker, M.D.

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Colorado researchers theorize that fructose metabolism may be the driving force behind Alzheimer Disease pathology. Diets high in sugar and high glycemic index carbohydrates would exacerbate the problem. Salt may also play a role. Fructose is a simple sugar (a monosaccharide) typically found in fruit, honey, and some vegetables. Table sugar is sucrose, a combination of fructose with a glucose molecule. High-fructose corn syrup (HFCS) is added to many processed foods as a sweetener. From the article linked above:

An ancient human foraging instinct, fueled by fructose production in the brain, may hold clues to the development and possible treatment of Alzheimer’s disease (AD), according to researchers at the University of Colorado Anschutz Medical Campus.

The study, published recently in The American Journal of Clinical Nutrition, offers a new way of looking at a fatal disease characterized by abnormal accumulations of proteins in the brain that slowly erode memory and cognition.

“We make the case that Alzheimer’s disease is driven by diet,” said the study’s lead author Richard Johnson, MD, professor at the University of Colorado School of Medicine specializing in renal disease and hypertension. The study co-authors include Maria Nagel, MD, research professor of neurology at the CU School of Medicine.

Steve Parker, M.D.

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I have nothing against Prilosec in particular. It can be very helpful.

We have two major classes of drugs that reduce acid production by the stomach. The first was H2 blockers, the granddaddy being Tagamet (cimetidine). Tagamet was the first PPI on the market in the U.S., probably 25-30 years ago. Several H2 blockers are are available without a prescription. The second and later class of acid-reducing drugs is the PPI. These are more potent than H2 blockers. Because of H2 blockers and PPIs, and the discovery that H. pylori causes many ulcers, we have many fewer patients requiring surgery for upper GI ulcers. Surgery like vagotomy and pyloroplasty. Once the ulcer heals, most folks don’t need to take a PPI for the rest of their lives.

There are reasons our stomachs produce acid. One is that the acid helps kill pathogens in our food before they make us sick. Another is to start the digestion of proteins we eat. You can imagine that drastically reducing stomach acid production has some potential adverse effects.

Bix at Fanatic Cook turned me on to the possibility that chronic use of  PPIs might cause cognitive decline, up to and including dementia. In the U.S., PPIs are available over-the-counter and many physicians prescribe and recommend them to patients in order to reduce stomach acid. The most common reason for chronic usage must be gastroesophageal reflux disease (aka GERD), which is severe or frequently recurrent heartburn. Common PPI names are Protonix, Nexium, Prilosec, omeprazole, and pantoprazole.

A German population study a few years ago linked PPI usage with higher risk of dementia.

A total of 73,679 participants 75 years of age or older and free of dementia at baseline were analyzed. The patients receiving regular PPI medication (n = 2950; mean [SD] age, 83.8 [5.4] years; 77.9% female) had a significantly increased risk of incident dementia compared with the patients not receiving PPI medication (n = 70,729; mean [SD] age, 83.0 [5.6] years; 73.6% female) (hazard ratio, 1.44 [95% CI, 1.36-1.52]; P < .001).

The avoidance of PPI medication may prevent the development of dementia. This finding is supported by recent pharmacoepidemiological analyses on primary data and is in line with mouse models in which the use of PPIs increased the levels of β-amyloid in the brains of mice. Randomized, prospective clinical trials are needed to examine this connection in more detail.

Source: Association of Proton Pump Inhibitors With Risk of Dementia: A Pharmacoepidemiological Claims Data Analysis – PubMed

Check out Bix’s article to read that:

• PPIs interfere with production of acetylcholine, a major chemical than nerve cells use to communicate with each other
• Healthy young folks who took a PPI for 10 days performed worse on tests of memory

I don’t know about Germany, but there’s evidence that the incidence of dementia has been decreasing lately in the U.S. I’m guessing that the use of PPIs has been increasing over the last couple decades. So this doesn’t fit with the PPI-dementia theory.

If you have GERD, a low-carb diet may well control it, allowing you to avoid the side effects of PPIs, not to mention the cost.

Oh, darn. I may not be getting my check from Big Pharma this month.

Steve Parker, M.D.

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Yes, some cases of dementia are preventable. If you have a genetic predisposition to develop dementia, the deck is stacked against you. But it’s not hopeless. A healthy lifestyle will help you, too.

The research at hand was done in the UK and involved over 500,000 older adults of European ancestry, free of dementia and cognitive impairment at baseline.

So what are the healthy lifestyle characteristics linked to lower risk of dementia, whether you have genetic risk or not?

• Physical activity
• Not smoking
• Healthy diet
• Judicious alcohol consumption

Lifestyle details from the research report:

A healthy lifestyle score was constructed based on 4 well-established dementia risk factors (smoking status, physical activity, diet, and alcohol consumption) assessed at baseline using a touchscreen questionnaire. Participants scored 1 point for each of 4 healthy behaviors defined on the basis of national recommendations (full details in eTable 1 in Supplement 1). Smoking status was categorized as current or no current smoking. Regular physical activity was defined as meeting the American Heart Association recommendations of at least 150 minutes of moderate activity per week or 75 minutes of vigorous activity per week (or an equivalent combination) or engaging in moderate physical activity at least 5 days a week or vigorous activity once a week. Healthy diet was based on consumption of at least 4 of 7 commonly eaten food groups following recommendations on dietary priorities for cardiometabolic health, which are linked to better late-life cognition and reduced dementia risk. Previous studies of alcohol consumption and dementia risk support a U-shaped relationship, with moderate consumption associated with lower risk. Therefore, moderate consumption was defined as 0 to 14 g/d for women and 0 to 28 g/d for men, with the maximum limit reflecting US dietary guidelines.

Source: Association of Lifestyle and Genetic Risk With Incidence of Dementia | Dementia and Cognitive Impairment | JAMA | JAMA Network

What do they consider a healthy dementia-preventing diet? At least four of the following food groups and consumption levels:

• Fruits: 3 or more servings a day
• Veggies: 3 or more servings a day
• Fish: 2 or more servings a week
• Processed meats: no more than 1 serving a week
• Unprocessed red meats: no more than 1.5 servings a week
• Whole grains: 3 or more servings a day
• Refined grains: no more than 1.5 servings a day

Regarding alcohol, the guideline is no more than one drink a day for women, and no more than two a day for men. “One drink” is 14 grams of pure alcohol. In human terms, one drink is 5 ounces of wine, 12 ounces of beer, or 1.5 ounces of 80 proof distilled spirits (e.g., vodka, whiskey, gin).

We don’t know if the paleo diet would help prevent dementia or not.

Steve Parker, M.D.

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Most cavemen didn’t live long enough to get dementia

Several respected researchers think that Alzheimer’s dementia may primarily be an infectious disease, particularly related to gum bacteria.

From MedScape:

LOS ANGELES — As more disappointing results emerge from anti-amyloid drug trials in Alzheimer’s disease (AD), there is growing interest in novel treatment approaches for this condition.

One such approach is based on the hypothesis that Porphyromonas gingivalis (Pg), the bacteria involved in periodontal disease, may cause AD. The biopharmaceutical company Cortexyme Inc is testing this theory with an investigational agent COR388, which targets gingipains, the toxic proteases released by Pg.  Early results show the drug is well tolerated and promising in terms of biomarker findings. Organizers hope that a phase 2/3 trial of the treatment now under way will provide definitive efficacy results.

Source: Gum Disease Bacteria a Novel Treatment Target for Alzheimer’s?

Steve Parker, M.D.

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HgbA1c (hemoglobin A1c) is measure of average blood sugar levels over the previous three months. From a 2018 study:

In this community-based population, we observed a significant trend for cognitive decline over a 10 year period among individuals aged ≥50 years with normoglycaemia, prediabetes or diabetes at baseline. Additionally, HbA1c levels were linearly associated with subsequent cognitive decline in memory and executive function (but not orientation) irrespective of diabetes status at baseline.

Source: HbA1c, diabetes and cognitive decline: the English Longitudinal Study of Ageing | SpringerLink

h/t to Jan at The Low-Carb Diabetic

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