Category: Anti-aging

In our continuing series on compounds that can have a positive impact on prevention of viral infections as well as improving response to infections today I want to highlight Vitamin D.

Vitamin D not only acts as a vitamin but also as a prohormone and it influences hundreds of biochemical processes in human physiology.

Following is a press release from the Orthomolecular Medicine News Service which provides details on how Vitamin D could reduce the risk of influenza and COVID-19 infection and death.

Copyright © 2020 Robert Lamberton

All rights reserved

FOR IMMEDIATE RELEASE
Orthomolecular Medicine News Service, Apr 9, 2020

Vitamin D Supplements Could Reduce Risk of Influenza and COVID-19 Infection and Death

by William B. Grant, PhD and Carole A. Baggerly

(OMNS Apr 9, 2020) There are two main reasons why respiratory tract infections such as influenza and COVID-19 occur in winter: winter sun and weather and low vitamin D status. Many viruses live longer outside the body when sunlight, temperature, and humidity levels are low as they are in winter [1].Vitamin D is an important component of the body’s immune system, and it is low in winter due to low solar ultraviolet-B (UVB) doses from exposure and the low supplement intakes of most. While nothing can be done about winter sun and weather, vitamin D status can be raised through vitamin D supplements.

Vitamin D has several mechanisms that can reduce risk of infections [2]. Important mechanisms regarding respiratory tract infections include:

  • inducing production of cathelicidins and defensins that can lower viral survival and replication rates as well as reduce risk of bacterial infection
  • reducing the cytokine storm that causes inflammation and damage to the lining of the lungs that can lead to pneumonia and acute respiratory distress syndrome.

Vitamin D deficiency has been found to contribute to acute respiratory distress syndrome, a major cause of death associated with COVID-19 [3]. An analysis of case-fatality rates in 12 U.S. communities during the 1918-1919 influenza pandemic found that communities in the sunny south and west had much lower case-fatality rates (generally from pneumonia) than those in the darker northeast [4].

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Continuing on with our discussion on strategies to help to protect against viruses in general and the SARS-CoV-2 virus in particular, today I want to highlight zinc.

As I have in previous posts, I want to make it clear that any of these recommendations I share are not intended to suggest that you should not access medical care if you suspect you may have contracted or been exposed to the SARS-CoV-2 virus – or any other serious illness.

Numerous clinical trials have clearly demonstrated that zinc is effective against viruses – including the common cold.

Some MDs have started to incorporate the use of zinc in a protocol which also includes Hydroxychloroquine – an old generation malaria drug with Azithromycin – an antibiotic.

In this anecdotal report from Vladimir (Zev) Zelenko MD who is based in Monroe, NY in his protocol he prescribed 200 mg of zinc sulfate per day for five days for active SARS-CoV-2 virus infections.

Typical zinc supplements are typically approximately 15 – 30 mg per day – this would be for ongoing health maintenance but not necessarily active viral infections.

Recent feedback has shown that the SARS-CoV-2 virus can initially become very active in the nose and throat areas and a zinc spray has traditionally been used for helping to target viral infections in these areas. Zinc sprays are often combined with other ingredients such as echinacea and they are available at most health food stores.

One consideration with respect to zinc consumption is that you need to be careful because there is a balance in the body between zinc and copper.

Some zinc supplements also include added copper – typically approximately 2 mg per day.

Consult a knowledgeable health care practitioner for more precise information on recommended dosages.

Zinc is another compound that we have available to help to maintain our state of health and to help to prevent viral infections – but also it can be a valuable tool for active infections.

There are many simple steps that can be taken to help protect oneself from the SARS-CoV-2 virus.

One of these would be to take some supplemental melatonin.

Melatonin levels decrease as we age and low melatonin levels may be a contributing factor as to why older individuals have more serious health issues with the virus if they become infected.

Melatonin provides many health benefits however one of the key ones as it pertains to the virus is it helps to prevent the cytokine cascade which is typical in those who develop lung damage.

The cytokine cascade is an overreaction of the immune system which can cause significant inflammation and result in the development of acute respiratory distress syndrome (ARDS) .

Here is a link to a good article on this topic from the

Deep Roots at Home website

So taking some melatonin in the evening – approximately 3- 5 mg about an hour before bed will not only help with your sleep but help to protect you from the SARS-CoV-2 virus.

  • IF you are taking ACE inhibitors, have cardiac conditions, hypertension, you need to consult your physician before taking high doses of melatonin.  Melatonin may lower blood pressure and cause hypotension at higher dosages.  
  • IF you are diabetic, or have insulin resistance, DO NOT TAKE MELATONIN before 3 pm.  Melatonin is able to suppress insulin. 

Today I want to share with you an article from the Hormones Matter website written by  Chandler Marrs, PhD

The article focuses on the fact that many individuals are consuming Metformin considering it to be a magical anti-aging drug.

I am in agreement with Chandra in that personally I have have never been a fan.

There are several considerations for myself as to why I feel this way which she talks about in this article, such as deficiencies that can develop, negative effects on mitochondrial function and a potential negative impact on exercise performance.

I would suggest that berberine provides many of the same benefits as Metformin as well as some such as CV benefits that Metformin does not provide – and berberine does not have any of the same negative effects vs. Metformin.

Following is Chandler’s article

I have never been a fan of Metformin. It seemed too good to be true. Many years ago I had a conversation with a researcher about all of its possible therapeutic indications. His lab was actively pursuing the anti-cancer angle. That should have been a clue that Metformin might be causing more damage than we recognized, but it wasn’t. At that point, I was still enamored with the wonders of pharmacology and hadn’t yet begun my path toward understanding medication adverse reactions. Indeed, it wasn’t until very recently, when a family member began suffering from one of these reactions, that I began my investigation in full. This is what I learned.

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Exposure to and accumulation of environmental toxins represents a major challenge to optimizing health in our current environment.

BPA – Bisphenol A is one of these environmental toxins which has received considerable coverage over the last several years.

The article I want to share with you today –from an article posted on the Science Daily website suggests that levels of accumulation in humans has been seriously underestimated.

This article was based upon a published study done at Washington State University and published in The Lancet Diabetes & Endocrinologythe citation is included at the end of this article.

Just before you read this information, here is an excerpt from an abstract on”Health Risk of Exposure to Bisphenol A” (abstract included at the end of this article) on some of the potential issues that exposure to BPA may cause:

” Due to its phenolic structure BPA has been shown to interact with estrogen receptors and to act as agonist or antagonist via estrogen receptor (ER) dependent signalling pathways. Therefore, BPA has been shown to play a role in the pathogenesis of several endocrine disorders including female and male infertility, precocious puberty, hormone dependent tumours such as breast and prostate cancer and several metabolic disorders including polycystic ovary syndrome (PCOS)”

Due to the prevalence of exposure to BPA in our environment – as well as other chemicals and heavy metals periodic monitoring and supervised detox programs to clear out this toxin load are serious considerations for optimizing health and potentially extending healthspan.

Summary:

  Researchers have developed a more accurate method of measuring bisphenol A (BPA) levels in humans and found that exposure to the endocrine-disrupting chemical is far higher than previously assumed. The study provides the first evidence that the measurements relied upon by regulatory agencies, including the US Food and Drug Administration, are flawed, underestimating exposure levels by as much as 44 times. Researchers have developed a more accurate method of measuring bisphenol A (BPA) levels in humans and found that exposure to the endocrine-disrupting chemical is far higher than previously assumed.

The study, published in the journal The Lancet Diabetes & Endocrinology on Dec. 5, provides the first evidence that the measurements relied upon by regulatory agencies, including the U.S. Food and Drug Administration, are flawed, underestimating exposure levels by as much as 44 times.

“This study raises serious concerns about whether we’ve been careful enough about the safety of this chemical,” said Patricia Hunt, Washington State University professor and corresponding author on the paper. “What it comes down to is that the conclusions federal agencies have come to about how to regulate BPA may have been based on inaccurate measurements.”

BPA can be found in a wide range of plastics, including food and drink containers, and animal studies have shown that it can interfere with the body’s hormones. In particular, fetal exposure to BPA has been linked to problems with growth, metabolism, behavior, fertility and even greater cancer risk.

Despite this experimental evidence, the FDA has evaluated data from studies measuring BPA in human urine and determined that human exposure to the chemical is at very low, and therefore, safe levels. This paper challenges that assumption and raises questions about other chemicals, including BPA replacements, that are also assessed using indirect methods.

Hunt’s colleague, Roy Gerona, assistant professor at University of California, San Francisco, developed a direct way of measuring BPA that more accurately accounts for BPA metabolites, the compounds that are created as the chemical passes through the human body.

Previously, most studies had to rely on an indirect process to measure BPA metabolites, using an enzyme solution made from a snail to transform the metabolites back into whole BPA, which could then be measured.

Gerona’s new method is able to directly measure the BPA metabolites themselves without using the enzyme solution.

In this study, a research team comprised of Gerona, Hunt and Fredrick vom Saal of University of Missouri compared the two methods, first with synthetic urine spiked with BPA and then with 39 human samples. They found much higher levels of BPA using the direct method, as much as 44 times the mean reported by the National Health and Nutrition Examination Survey (NHANES). The disparity between the two methods increased with more BPA exposure: the greater the exposure the more the previous method missed.

Gerona, the first author on the paper, said more replication is needed.

“I hope this study will bring attention to the methodology used to measure BPA, and that other experts and labs will take a closer look at and assess independently what is happening,” he said.

The research team is conducting further experiments into BPA measurement as well as other chemicals that may also have been measured in this manner, a category that includes environmental phenols such as parabens, benzophenone, triclosan found in some cosmetics and soaps, and phthalates found in many consumer products including toys, food packaging and personal care products.

“BPA is still being measured indirectly through NHANES, and it’s not the only endocrine-disrupting chemical being measured this way,” Gerona said. “Our hypothesis now is that if this is true for BPA, it could be true for all the other chemicals that are measured indirectly.”

This study was supported by grants from the National Institutes of Health.


Story Source:

Materials provided by Washington State University. Original written by Sara Zaske. Note: Content may be edited for style and length.


Journal Reference:

  1. Roy Gerona, Frederick S vom Saal, Patricia A Hunt. BPA: have flawed analytical techniques compromised risk assessments? The Lancet Diabetes & Endocrinology, 2019; DOI: 10.1016/S2213-8587(19)30381-X

Rocz Panstw Zakl Hig. 2015;66(1):5-11.

Health risk of exposure to Bisphenol A (BPA).

Konieczna A1, Rutkowska A1, Rachoń D1.  

Abstract

Bisphenol A (BPA) belongs to chemicals that are produced in large quantities worldwide. It is commonly used as monomer in polycarbonate synthesis, plasticizer in the production of epoxy resins, as well as an additive for the elimination of surfeit of hydrochloric acid during the polyvinyl chloride (PVC) production. BPA is not only used in the production of plastics intended to a direct contact with food, including plastic packaging and kitchenware, but also in inner coatings of cans and jar caps. There are various routes of human exposure to this substance such as oral, by inhalation and transdermal. The main sources of exposure to BPA include food packaging and dust, dental materials, healthcare equipment, thermal paper, toys and articles for children and infants. BPA is metabolized in the liver to form bisphenol A glucuronide and mostly in this form is excreted with urine. Due to its phenolic structure BPA has been shown to interact with estrogen receptors and to act as agonist or antagonist via estrogen receptor (ER) dependent signalling pathways. Therefore, BPA has been shown to play a role in the pathogenesis of several endocrine disorders including female and male infertility, precocious puberty, hormone dependent tumours such as breast and prostate cancer and several metabolic disorders including polycystic ovary syndrome (PCOS).

Because of the constant, daily exposure and its tendency to bio-accumulation, BPA seems to require special attention such as biomonitoring. This observation should include clinical tests of BPA concentration in the urine, which is not only one of the best methods of evaluation of the exposure to this compound, but also the dependence of the daily intake of BPA and the risk of some endocrine disorders. PMID: 25813067

Dietary intervention restores protective protein and decreases death rate in mice

Source: Society for Neuroscience

The incidence of dementia and Alzheimer’s continues to escalate in the general population.

LCHF/Keto diets have proven to be beneficial to individuals dealing with these health issues.

It has been suggested that these conditions may partly be due to impaired glucose metabolism in the brain, hence the increasing use of the term “Type 3 Diabetes”.

Enabling the brain to use ketones for its energy source therefore can provide some benefit with regards to brain function.

A major challenge with this is that a radical dietary shift in the geriatric population can be quite challenging – if not impossible.

Usage of exogenous ketone compounds is one potential option in this situation.

Following is an article from Science Daily which talks about published research which suggests that increasing ketone levels in the diet can help to protect neurons from death during the progression of Alzheimer’s disease.

Summary: A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice.

A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice recently published in JNeurosci.

Early in the development of Alzheimer’s disease, the brain becomes over excited, potentially through the loss of inhibitory, or GABAergic, interneurons that keep other neurons from signaling too much. Because interneurons require more energy compared to other neurons, they may be more susceptible to dying when they encounter the Alzheimer’s disease protein amyloid beta. Amyloid beta has been shown to damage mitochondria — the metabolic engine for cells — by interfering with SIRT3, a protein that preserves mitochondrial functions and protects neurons.

Cheng et al. genetically reduced levels of SIRT3 in mouse models of Alzheimer’s disease. Mice with low levels of SIRT3 experienced a much higher mortality rate, more violent seizures, and increased interneuron death compared to the mice from the standard Alzheimer’s disease model and control mice. However, the mice with reduced levels of SIRT3 experienced fewer seizures and were less likely to die when they ate a diet rich in ketones, a specific type of fatty acid. The diet also increased levels of SIRT3 in the mice.

Increasing SIRT3 levels via ketone consumption may be a way to protect interneurons and delay the progression of Alzheimer’s disease.


Story Source:

Materials provided by Society for Neuroscience. Note: Content may be edited for style and length.


Journal Reference:

  1. Aiwu Cheng, Jing Wang, Nathaniel Ghena, Qijin Zhao, Isabella Perone, M. Todd King, Richard L. Veech, Myriam Gorospe, Ruiqian Wan, Mark P. Mattson. SIRT3 Haploinsufficiency Aggravates Loss of GABAergic Interneurons and Neuronal Network Hyperexcitability in an Alzheimer’s Disease Model. The Journal of Neuroscience, 2019; 1446-19 DOI: 10.1523/JNEUROSCI.1446-19.2019

Abstract

SIRT3 Haploinsufficiency Aggravates Loss of GABAergic Interneurons and Neuronal Network Hyperexcitability in an Alzheimer’s Disease Model

Impaired mitochondrial function and aberrant neuronal network activity are believed to be early events in the pathogenesis of Alzheimer’s disease (AD), but how mitochondrial alterations contribute to aberrant activity in neuronal circuits is unknown. In this study, we examined the function of mitochondrial protein deacetylase sirtuin 3 (SIRT3) in the pathogenesis of AD. Compared to AppPs1 mice, Sirt3-haploinsufficient AppPs1 mice (Sirt3+/-AppPs1) exhibit early epileptiform EEG activity and Seizure. Both male and female Sirt3+/-AppPs1 mice were observed to die prematurely before five months of age.

When comparing male mice among different genotypes, Sirt3 haploinsufficiency renders GABAergic interneurons in the cerebral cortex vulnerable to degeneration and associated neuronal network hyperexcitability. Feeding Sirt3+/-AppPs1 AD mice with a ketone ester-rich diet increases SIRT3 expression and prevents seizure-related death and the degeneration of GABAergic neurons, indicating that the aggravated GABAergic neuron loss and neuronal network hyperexcitability in Sirt3+/-AppPs1 mice are caused by SIRT3 reduction and can be rescued by increase of SIRT3 expression. Consistent with a protective role in AD, SIRT3 levels are reduced in association with cerebral cortical Aβ pathology in AD patients. In summary, SIRT3 preserves GABAergic interneurons and protects cerebral circuits against hyperexcitability, and this neuroprotective mechanism can be bolstered by dietary ketone esters.

SIGNIFICANCE STATEMENT

GABAergic neurons provide the main inhibitory control of neuronal activity in the brain. By preserving mitochondrial function, SIRT3 protects parvalbumin and calretinin interneurons against Aβ-associated dysfunction and degeneration in AppPs1 AD mice, thus restraining neuronal network hyperactivity. The neuronal network dysfunction that occurs in AD can be partially reversed by physiological, dietary, and pharmacological interventions to increase SIRT3 expression and enhance the functionality of GABAergic interneurons.