Keto diet overcomes unfavorable ApoE4 Alzheimer's genetics

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Wiki Rostas

Wiki Fish

... better way to put it - ketogenic diet renders some of the genetical conditions such as ApoE4+  irrelevant or not endangering an individual survival chances! It appears ApoE4+ does represent a handicap ONLY on a high carbohydrate diet! It is probably similar with many other genetic impairments. It seems one needs to have a more than "perfect" genetics to be able to remain healthy until a very old age on a high carbohydrate diet!

"Ketogenic diet rescues cognition in ApoE4+ patient with mild Alzheimer's disease: A case study.", by Morrill SJ, Gibas KJ, Diabetes Metab Syndr., March-April 2019


Quotes:

Abstract
It has been established that there is a correlation between Alzheimer's disease and apolipoprotein E, specifically the ApoE4 genetic variant. However, the correlation between Apoe4, insulin resistance and metabolic syndrome (MetS) pathologies still remains elusive. As apolipoprotein E has many important physiological functions, individuals with the ApoE4 allele variant, also known as the Alzheimer's disease gene, are primarily at a greater risk for physiological consequences, specifically cognitive impairment (Chan et al., 2016). In this case study, a 71-year old female, heterozygous for ApoE4 with a family history of Alzheimer's Disease (AD) and the dual diagnosis of mild AD/metabolic syndrome (MetS) was placed on a 10-week nutrition protocol purposed at raising plasma ketones through carbohyrdrate restricted, high fat ketogenic diet (KD), time- restricted eating and physical/cognitive exercise. Primary biomarkers for MetS were measured pre/mid-/post intervention. The MoCA (Montreal Cognitive Assessment) was administered pre/post intervention by a licensed clinical therapist. The results were statistically significant. The HOMA-IR decreased by 75% from 13.9 to 3.48. Triglycerides decreased by 50% from 170mg/dL to 85mg/dL. VLDL dropped by 50% from 34mg/dL to 17mg/dL, and HgA1c decreased from 5.7% to 4.9%. The baseline MoCA score was 21/30; post treatment score was 28/30. The significant results in both MetS biomarkers and the MoCA score suggest that a ketogenic diet may serve to rescue cognition in patients with mild AD. The results of this case study are particularly compelling for ApoE4 positive (ApoE4+) subjects as ketogenic protocols extend hope and promise for AD prevention.

UPDATE

Within a short time from posting the above, the following comments were posted on Twitter.
(BTW - Thanks Tucker Goodrich and Shaza!)

Indeed, it turns out that it is not the keto diet per-se but rather the improved DHA contents of such a diet that is the critical factor, not just the low carbohydrates aspect of it!    Tsimane (Bolivian natives) diet is high carbohydrate (vegetable & fruit) and low protein (16%), low fat but also most of the protein comes from fish.  The paper on "DHA brain uptake..." of ApoE4 versus non-ApoE4 carriers confirms that the critical factor is abundance of DHA in food for the ApoE4 carriers. In return they have a higher mass of grey matter in the brain than non-ApoE4, which appears to be confirmed by cognition tests [add study refs]. In return for having higher grey matter mass, the uptake of DHA is 20% higher for ApoE4 carriers, making them more vulnerable to DHA starvation.

It seems that this story has evolved in a direction that I did not expect. Perhaps the ApoE4 rather than being a mildly inconvenient adaptation requiring high fat/high fish diet, turns out to be a very beneficial genetic evolutionary trait helping in brain development and achieving higher IQ - which is clearly a survival advantage. Especially for navigation over the high seas or in the Arctic!

Nuts against dementia

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Study: A Daily Dose Of Nuts Could Be Key To Staying Sharp In Old Age

From Wiki Nut (fruit)-
By Sage Ross- Own work,
CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=30392736

Study release report (March 2019):

A nutty solution for improving brain health

Quote:

Long-term, high nut consumption could be the key to better cognitive health in older people according to new research from the University of South Australia.

In a study of 4822 Chinese adults aged 55+ years, researchers found that eating more than 10 grams of nuts a day was positively associated with better mental functioning, including improved thinking, reasoning and memory.

Lead researcher, UniSA’s Dr Ming Li, says the study is the first to report an association between cognition and nut intake in older Chinese adults, providing important insights into increasing mental health issues (including dementia) faced by an ageing population.

“Population aging is one of the most substantial challenges of the twenty-first century. Not only are people living longer, but as they age, they require additional health support which is placing unprecedented pressure on aged-care and health services,” Dr Li says.

Reference:

A Prospective Association of Nut Consumption with Cognitive Function in Chinese Adults Aged 55+ _ China Health and Nutrition Survey

Connection between immune system, microbiome and psychiatric disorders

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"He Got Schizophrenia. He Got Cancer. And Then He Got Cured." by Moises Velasquez-Manoff, NYT, Sept. 29, 2018

Quotes:

...A year later, the man’s condition worsened. He developed fatigue, fever and shortness of breath, and it turned out he had a cancer of the blood called acute myeloid leukemia. He’d need a bone-marrow transplant to survive. After the procedure came the miracle. The man’s delusions and paranoia almost completely disappeared. His schizophrenia seemingly vanished.

Years later, “he is completely off all medication and shows no psychiatric symptoms,” Dr. Miyaoka told me in an email. Somehow the transplant cured the man’s schizophrenia.

A bone-marrow transplant essentially reboots the immune system. Chemotherapy kills off your old white blood cells, and new ones sprout from the donor’s transplanted blood stem cells. It’s unwise to extrapolate too much from a single case study, and it’s possible it was the drugs the man took as part of the transplant procedure that helped him. But his recovery suggests that his immune system was somehow driving his psychiatric symptoms.

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In the late 19th century, physicians noticed that when infections tore through psychiatric wards, the resulting fevers seemed to cause an improvement in some mentally ill and even catatonic patients.

Inspired by these observations, the Austrian physician Julius Wagner-Jauregg developed a method of deliberate infection of psychiatric patients with malaria to induce fever. Some of his patients died from the treatment, but many others recovered. He won a Nobel Prize in 1927.

One much more recent case study relates how a woman’s psychotic symptoms — she had schizoaffective disorder, which combines symptoms of schizophrenia and a mood disorder such as depression — were gone after a severe infection with high fever.

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Indeed, in the past 15 years or so, a new field has emerged called autoimmune neurology. Some two dozen autoimmune diseases of the brain and nervous system have been described. The best known is probably anti-NMDA-receptor encephalitis, made famous by Susannah Cahalan’s memoir “Brain on Fire.” These disorders can resemble bipolar disorder, epilepsy, even dementia — and that’s often how they’re diagnosed initially. But when promptly treated with powerful immune-suppressing therapies, what looks like dementia often reverses. Psychosis evaporates. Epilepsy stops. Patients who just a decade ago might have been institutionalized, or even died, get better and go home.

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Dr. Robert Yolken, a professor of developmental neurovirology at Johns Hopkins, estimates that about a third of schizophrenia patients show some evidence of immune disturbance. “The role of immune activation in serious psychiatric disorders is probably the most interesting new thing to know about these disorders,” he told me.

Studies on the role of genes in schizophrenia also suggest immune involvement, a finding that, for Dr. Yolken, helps to resolve an old puzzle. People with schizophrenia tend not to have many children. So how have the genes that increase the risk of schizophrenia, assuming they exist, persisted in populations over time? One possibility is that we retain genes that might increase the risk of schizophrenia because those genes helped humans fight off pathogens in the past. Some psychiatric illness may be an inadvertent consequence, in part, of having an aggressive immune system.

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Another case study from the Netherlands highlights this still-mysterious relationship. In this study, on which Dr. Yolken is a co-author, a man with leukemia received a bone-marrow transplant from a schizophrenic brother. He beat the cancer but developed schizophrenia. Once he had the same immune system, he developed similar psychiatric symptoms.

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And there may be other, softer interventions. A decade ago, Dr. Miyaoka accidentally discovered one. He treated two schizophrenia patients who were both institutionalized, and practically catatonic, with minocycline, an old antibiotic usually used for acne. Both completely normalized on the antibiotic. When Dr. Miyaoka stopped it, their psychosis returned. So he prescribed the patients a low dose on a continuing basis and discharged them.

Minocycline has since been studied by others. Larger trials suggest that it’s an effective add-on treatment for schizophrenia. Some have argued that it works because it tamps down inflammation in the brain. But it’s also possible that it affects the microbiome — the community of microbes in the human body — and thus changes how the immune system works.

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The study is preliminary, but it suggests that targeting immune function may improve mental health outcomes and that tinkering with the microbiome might be a practical, cost-effective way to do this.