statins and cholesterol scam

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Do statins really work? Who benefits? Who has the power to cover up the side effects?,
By Aseem Malhotra , European Scientist - 03.09.2019,

Wiki

Quote:

Why It’s now time for a full public parliamentary inquiry into the controversial drug and fully expose the great cholesterol and statin con

Earlier this week, the Chair of the British Parliament Science and Technology Committee, Sir Norman Lamb MP made calls for a full investigation into cholesterol lowering statin drugs. It was instigated after a letter was written to him signed by a number of eminent international doctors including the editor of the BMJ, the Past President of the Royal College of Physicians and the Director of the Centre of Evidence Based Medicine in Brazil wrote a letter calling for a full parliamentary inquiry into the controversial medication[1]. It’s lead author Cardiologist Dr Aseem Malhotra makes the case for why’s there’s an urgent need for such an investigation in European Scientist.

A few weeks ago, an alarmed and confused patient in his late forties, who I shall call Mr Smith, came to see me for a consultation. Four years earlier he suffered a heart attack where severe blockages were found in his right coronary artery. These were opened up and kept open with metal stents.

He was prescribed atorvastatin, which is standard practice for heart attack patients regardless of cholesterol levels. Unfortunately, the atorvastatin caused severe muscle pains on exercise. Fortunately, his symptoms disappeared within a week of stopping the drug.

As an alternative to his statin, he decided to adopt an ultra-low fat vegan diet which he believed may halt, even reverse heart disease through lowering cholesterol. Within months he dropped his total cholesterol by 40% from 5.2mmol/L to 3.2, now placing his levels in the bottom five per cent of the population.

Despite sticking religiously to the diet, he began to develop chest pain when he did exercise, and a repeat heart scan showed a seventy per cent blockage in another artery, one that had been completely clear four years before. “How is this possible?” he asked me, clearly upset. ‘How could I develop more heart disease in such a short space of time with such low cholesterol?’

I explained to him his case was not unusual, nor inexplicable.
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Rather than accept greater scrutiny, highly influential cardiologists are attacking those who question the benefits of statins. Those who believed that side effects are much more prevalent are denounced as peddlers of “fake news” or “fake science”. They are compared to “anti – vaxxers”.One Cardiologist, Ana Navar even wrote in a recent editorial in JAMA Cardiology that inappropriate fears about statin side effects are coming from social media wellness bloggers and that “lives lost from inappropriate concerns about statins may number in the millions” but this is not evidence based. The side effect literature and remarkably high discontinuation rate comes from very credible sources[21].

The largest statin survey in the United States exposes 75% of those prescribed the medication stop it within a year of prescription with 62% of those stating side effects as the reason

Even as far back as 2002 when there was no social media or public awareness of statin side effects a paper in JAMA of over 40,000 patients reveals that 60% of heart attack patients aged over 65 will stop the drug within 2 years (ref)

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So how effective are statins in preventing and treating heart disease?

When one removes the industry funded PR and hype, the results are pretty underwhelming.

In 2015, new research published in BMJ Open revealed that despite tens of millions more people being prescribed statins across many European countries there was no evidence that this had any effect on cardiovascular mortality, over a twelve year period[24].

If you strip down the statin trials to their moving parts, the data actually reveals that, even in those who have established heart disease, the benefits are very small. Even in this high risk group, the average increase in life expectancy from taking the drug religiously for five years is a meagre four days[25].

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We continue to have an epidemic of misinformed doctors and misinformed and unwittingly deceived and harmed patients. In large part this has been driven by a multi-billion-dollar food and drug industry that profits from the fear of cholesterol.

It’s now time for a full public parliamentary inquiry to push for the raw data on statins find out who really benefits, and to determine who has been manipulating and hiding data on the debilitating side effects that appear to possibly affect almost half taking the drug. Until then it’s better we focus healthcare resources in tackling the real root cause of heart disease through prioritising lifestyle changes. It’s finally time to stop falling for the great cholesterol and statin con.

Short-sightedness may be tied to high-carbohydrate diet

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Old but actual.

New Scientist article:

"Short-sightedness may be tied to refined diet", By Douglas Fox, 5 April 2002

Based on Wiki Eye

Quote:

Diets high in refined starches such as breads and cereals increase insulin levels. This affects the development of the eyeball, making it abnormally long and causing short-sightedness, suggests a team led by Loren Cordain, an evolutionary biologist at Colorado State University in Fort Collins, and Jennie Brand Miller, a nutrition scientist at the University of Sydney.

The theory could help explain the dramatic increase in myopia in developed countries over the past 200 years. It now affects 30 per cent of people of European descent, for example.

“The rate of starch digestion is faster with modern processed breads and cereals,” says Brand Miller. In response to this rapid digestion, the pancreas pumps out more insulin. High insulin is known to lead to a fall in levels of insulin-like binding protein-3, the team points out.

That could disturb the delicate choreography that normally coordinates eyeball lengthening and lens growth. And if the eyeball grows too long, the lens can no longer flatten itself enough to focus a sharp image on the retina, they suggest.

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But while reading may play a role, it does not explain why the incidence of myopia has remained low in societies that have adopted Western lifestyles but not Western diets, says Cordain.

“In the islands of Vanuatu they have eight hours of compulsory schooling a day,” he says, “yet the rate of myopia in these children is only two per cent.” The difference is that Vanuatuans eat fish, yam and coconut rather than white bread and cereals.

The theory is also consistent with observations that people are more likely to develop myopia if they are overweight or have adult-onset diabetes, both of which involve elevated insulin levels. The progression of myopia has also been shown to be slower in children whose protein consumption is increased.

Journal reference: Acta Ophthalmologica Scandinavica (vol 80, p 125)

aspirin reduces the risk of death by 16-19%

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"Association of Aspirin Use With Mortality Risk Among Older Adult Participants in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial", by Holli A. Loomans-Kropp, et al.,
JAMA Netw Open. 2019;2(12); published December 4, 2019

Quote:

Findings
This cohort study included 146152 individuals from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial and found that aspirin use 3 or more times per week was associated with reduced risk of all-cause, cancer, gastrointestinal cancer, and colorectal cancer mortality.

Results
A total of 146152 individuals (mean [SD] age at baseline, 66.3 [2.4] years; 74742 [51.1%] women; 129446 [88.6%] non-Hispanic white) were included in analysis. The median (interquartile range) follow-up time was 12.5 (8.7-16.4) years, encompassing 1822164 person-years. Compared with no use, aspirin use 1 to 3 times per month was associated with reduced risk of all-cause mortality (HR, 0.84; 95% CI, 0.80-0.88; P less than .001) and cancer mortality (HR, 0.87; 95% CI, 0.81-0.94; P less than .001). Aspirin use 3 or more times per week was associated with decreased risk of mortality of all causes (HR, 0.81; 95% CI, 0.80-0.83; P less than .001), any cancer (HR, 0.85; 95% CI, 0.81-0.88; P less than .001), GI cancer (HR, 0.75; 95% CI, 0.66-0.84; P less than .001), and CRC (HR, 0.71; 95% CI, 0.61-0.84; P less than .001).

Some people with schizophrenia may simply have B3 deficiency

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Some People With Schizophrenia May Simply Have a Vitamin Deficiency

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The idea behind the hypothesis occurred to Esme Fuller-Thomson, professor at the University of Toronto’s Factor-Inwentash Faculty of Social Work (FIFSW) after learning about recent research conducted in South India. This study newly identified a link between schizophrenia and a variant of the gene NAPRT1, which lowers the body’s ability to use niacin, or Vitamin B3, which naturally occurs in meat, poultry, fish, and eggs.

“When I read this study a light bulb went on in my head,” says Fuller-Thomson, who published the hypothesis in the journal Schizophrenia Research this month with doctoral student, Rukshan Mehta. “This seems to be the missing link that explains all these medical mysteries.”

The researchers speculate that there is a critical interaction between an expectant mother’s prenatal niacin deficiency due to malnourishment and the NAPRT1 variant that impedes the fetus’ ability to use niacin. This interaction between the gene and the prenatal environment may predispose the offspring to develop a psychotic disorder.

Several studies indicate that the offspring of mothers who experience famine in their first trimester of pregnancy have double the chance of developing schizophrenia. Most researchers assume nutrient deficiency must be playing a role, but the particular nutrient has yet to be identified. Fuller Thomson now speculates that niacin may be the key nutrient involved.

Note that there is also a connection with the ketogenic diet.

Since NAPRT1 (Nicotinate phosphoribosyltransferase) is essential for increasing cellular NAD levels (preventing also oxidative stress of cells)
and NAD is also a precursor to SIRT6 which is also critical in DNA repair (thus longevity!)

See also


NAPRT1 (Nicotinate phosphoribosyltransferase) is essential for increasing cellular NAD levels and, thus, to prevent oxidative stress of cells. NAPRT1 converts Nicotinic acid (NA; niacin) to NA mononucleotide (NaMN), which is then converted to NA adenine dinucleotide (NaAD), and finally to nicotinamide adenine dinucleotide (NAD)

Ketogenic diet slows progression of 5 neuro degenerative diseases

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Source reference paper:

Letter to the editor/
Could a gene-environment interaction between NAPRT1 risk allele and pre-natal niacin deficiency explain 4 medical mysteries of schizophrenia research?/
Esme Fuller-Thomson, Rukshan Mehta; Schizophrenia Research
Available online 12 December 2019