Since late 2016 we have entered the age of disclosures! Fasten your mental safety belt and enjoy the ride! Heretic

Sunday, April 14, 2019

People with low cholesterol dying like flies


"Serum total cholesterol and risk of cardiovascular and non-cardiovascular mortality in old age: a population-based study", Yajun LiangEmail author, Davide Liborio Vetrano and Chengxuan QiuEmail,
BMC Geriatrics, 2017/17:294

First graph from the above paper.



During 23,196 person-years of follow-up (median per person, 7.5 years), 1059 (34.3%) participants died. Compared to normal total cholesterol (<5.18 mmol/l), borderline-high (5.18-6.21 mmol/l) and high (≥6.22 mmol/l) total cholesterol were associated with a decreased risk of all-cause mortality, with the multiple-adjusted hazard ratio (95% confidence interval, CI) of 0.71 (0.61–0.83) and 0.68 (0.57–0.80), respectively (P for trend <0.001). The competing risk regression models revealed that the reduced all-cause mortality associated with high total cholesterol (≥6.22 mmol/l)) was mainly due to the reduced risk of non-cardiovascular mortality (hazard ratio = 0.67, 95% CI = 0.51-0.88). These associations were statistically evident only among individuals without use of cholesterol-lowering medications.


The inverse association between high total cholesterol and reduced all-cause mortality in older adults is primarily due to non-cardiovascular mortality, especially among those who are not treated with cholesterol-lowering medications.

Saturday, April 13, 2019

Telomere length correlates with red meat consumption

Blog article:

Unexpected relationship between Red Meat Diet and PBMC Telomere Length, Sep 28, 2016 1:30:54 AM / by Stacy Matthews Branch, DVM, PhD

Update 15-Jan-2020

500% extension for C.Elegans by TOR and Insulin IIS signaling modification:
Pathways that extend lifespan by 500 percent identified Discovery of cellular mechanisms could open door to more effective anti-aging therapies, Date:January 8, 2020, Mount Desert Island Biological Laboratory

The new research uses a double mutant in which the insulin signaling (IIS) and TOR pathways have been genetically altered. Because alteration of the IIS pathways yields a 100 percent increase in lifespan and alteration of the TOR pathway yields a 30 percent increase, the double mutant would be expected to live 130 percent longer. But instead, its lifespan was amplified by 500 percent.


"The relationship between peripheral blood mononuclear cells telomere length and diet - unexpected effect of red meat.", Kasielski M, Eusebio MO, Pietruczuk M, Nowak D., Nutr J. 2016 Jul 14;15(1)
Fig.1 from the paper above.

Mount Desert Island Biological Laboratory. "Pathways that extend lifespan by 500 percent identified: Discovery of cellular mechanisms could open door to more effective anti-aging therapies." ScienceDaily. ScienceDaily, 8 January 2020.

Jianfeng Lan, Jarod A. Rollins, Xiao Zang, Di Wu, Lina Zou, Zi Wang, Chang Ye, Zixing Wu, Pankaj Kapahi, Aric N. Rogers, Di Chen. Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity. Cell Reports, 2019; 28 (4): 1050 DOI: 10.1016/j.celrep.2019.06.078

Sunday, April 7, 2019

Schizophrenia put into remission on keto diet


Chronic Schizophrenia Put Into Remission Without Medication/New research suggests ketogenic diet may play a role in treating schizophrenia.
by Chris Palmer, M.D., Apr 06, 2019


An 82 year old woman with chronic paranoid schizophrenia since age 17

The first patient documented in the Schizophrenia Research article is a woman who spent nearly her whole life suffering chronic, treatment-resistant schizophrenia. For more than 50 years, she endured paranoia, disorganized speech, visual and auditory hallucinations. By the time she was 70, she was suicidal and had been hospitalized repeatedly for psychosis or suicide attempts. She had been treated with over ten different antipsychotic and mood stabilizing medications, including regular antipsychotic injections. None of them helped her symptoms. She was unable to care for herself and had a court-appointed guardian and home health services.

At the age of 70, weighing 330 pounds, she went to a medical weight loss clinic and was started on a ketogenic diet. Within two weeks of starting the diet, she reported a noticeable reduction not only in her weight but also her psychotic symptoms. Within several months, she started to feel so much better that she was able to stop taking her psychiatric medications while remaining on the diet. Over time, her mood stabilized, and her hallucinations and paranoia remitted completely. She was no longer suicidal. Her case was first reported in 2009.

Today, 12 years later, she has lost a total of 150 pounds and remains on the ketogenic diet. She takes no medications and remains symptom-free. She was able to regain her independence, no longer requiring the guardian and the home health care team. When I recently spoke with her, she recalled her decades of suffering and hopelessness, and said that since starting the diet, she has had a "new life," and is happy to be alive.

A 39 year old woman with schizophrenia for 20 years

The second patient described in the article is a thirty-nine year old woman who suffered from depression, anxiety, anorexia nervosa, hallucinations and paranoia since her teens. As patients sometimes do, she concealed her psychotic symptoms when she was initially treated for depression and anorexia. When she finally reported her psychotic symptoms later in her twenties, she was diagnosed with schizophrenia. For the next ten years, she was treated with 7 different antipsychotic medications—including clozapine (called the “gold standard antipsychotic medication”) - along with antidepressants and anti-anxiety medications. Nevertheless, she continued to have symptoms.

She was having chronic gastrointestinal problems, so she saw a doctor who recommended the ketogenic diet. Noticing some improvement of her symptoms and being frustrated with all of her psychiatric medications, she unwisely stopped taking all 14 of her medications “cold turkey.” This sent her into severe psychosis requiring an extended hospitalization. In the hospital, she was re-medicated with Haldol-decanoate (an injectable medication which had not worked for her previously) and she continued the ketogenic diet. Within a month on both Haldol and the ketogenic diet, she reported complete remission of her psychotic symptoms for the first time since she was 14. Over the following year, she slowly tapered off Haldol, and remained free of psychotic symptoms. Of note, she lost 70 pounds from the diet, which exacerbated her anorexia. She has since regained 30 of those pounds and maintains a healthy weight today. 5 years after starting the ketogenic diet, she is off all antipsychotic medications, remains on the diet, and is free of all psychotic symptoms. She has since finished graduate school and now works full time.

Interestingly, these aren’t the first reports of the ketogenic diet for schizophrenia
While inspiring, these two case reports join a growing body of evidence supporting the use of the ketogenic diet in the treatment of schizophrenia.

Schizophrenia in 1965

In 1965, ten women hospitalized with schizophrenia who were already receiving medications and electroconvulsive therapy (ECT or “shock therapy”) were also placed on the ketogenic diet for a month. The researchers reported that their symptoms improved after two weeks on the diet, but then returned back to their baseline level of symptoms after the diet was stopped.

Schizoaffective disorder in 2017

In 2017, I reported two other cases of schizoaffective disorder improving significantly on the ketogenic diet. Schizoaffective disorder is a diagnosis that includes both a mix of schizophrenia and a mood disorder, often bipolar disorder. One man and one woman, both in their 30’s, had suffered treatment-resistant schizoaffective disorder for years. On the diet, their symptoms were greatly improved, and they both lost significant amounts of weight. Off the diet, their symptoms returned.

Schizophrenia in Ecuador

In 2018, two Ecuadorian twins, one male and one female, diagnosed with schizophrenia since the ages of 14 and 18 were started on a 6-week trial of the ketogenic diet. This study had a psychiatrist rate each twin’s symptoms while being unaware of their diet status. Interestingly, only when the patients were compliant with the diet did their symptoms improve. They also both lost weight. When they stopped the diet at the end of the study, their symptoms returned to their baseline level.

Stan's comments: - who were the medical criminals who stopped their patients' treatment as the article described, in spite of the clear improvement and despite of no viable alternatives? Why there was no information published and made available over the years, to other patients suffering from this debilitating disease, and their families? It is very symptomatic of a very serious disease rotting the medical system from within, in all countries. What have the government departments in charge of public health policies done to make that treatment available? Why did the judicial system refrain from punishing the people involved in maintaining this information hidden or even actively discouraging it by denigrating all ketogenic diets, all high fat low carbohydrate diets publicly and in the media? Who were the people, and who financed those who campaigned in the media smearing Drs. Yudkin, Atkins, Bernstein and others and why did public prosecutors and politicians allowed that to continue?

More connections between metabolic disorder and psychiatric/neurological conditions:

"Impaired insulin signaling in unaffected siblings and patients with first episode psychosis", by Virginie-Anne Chouinard et al., Mol Psychiatry. 2018 Mar 9


Patients with psychotic disorders are at high risk for type 2 diabetes mellitus, and there is increasing evidence that patients display glucose metabolism abnormalities before significant antipsychotic medication exposure. In the present study, we examined insulin action by quantifying insulin sensitivity in first episode psychosis (FEP) patients and unaffected siblings, compared to healthy individuals, using a physiological-based model and comprehensive assessment battery. Twenty-two unaffected siblings, 18 FEP patients and 15 healthy unrelated controls were evaluated using a 2-hour oral glucose tolerance test (OGTT), with 7 samples of plasma glucose and serum insulin concentration measurements. Insulin sensitivity was quantified using the oral minimal model method. Lipid, leptin, free fatty acids and inflammatory marker levels were also measured. Anthropometric, nutrient and activity assessments were conducted; total body composition and fat distribution were determined using whole-body dual energy x-ray absorptiometry. Insulin sensitivity significantly differed among groups (F=6.01, P=0.004), with patients and siblings showing lower insulin sensitivity, compared to controls (P=0.006, and P=0.002, respectively).

Comment: Comparison between people diagnosed with psychiatric disorder and their sibling who were not diagnosed and therefore not affected by psychiatric drugs, showed the common underlying metabolic disorder involving insulin insensitivity and high risk of developing diabetes type 2.

Update 11/04/2019 Another interesting paper on this subject. A different angle:

"Psychosis and Symbiosis: Microbiome and Schizophrenia. Fascinating new research links the gut and brain in sickness and health.", by Emily Deans M.D., Posted Mar 31, 2019


Those mice that received the transplants from schizophrenic patients had higher levels of glutamine in the serum and hippocampus, decreased glutamate in the hippocampus, and increased GABA in the hippocampus. These difference were localized to areas of the brain particularly rich in glutamate and its metabolites (i.e., the outer shell of the brain and the hippocampus). This means that a transplant of a different microbiome led to different GABA-glutamate-glutamine neurotransmission in mouse brains. Corresponding human brain areas are related to memory, neuron repair, and executive functioning, all significantly impacted in schizophrenia.

In addition, the schizophrenia microbiome recipient mice had different behaviors than the healthy control mice, with exaggerated startle response and increased activity.