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Posted by: | Posted on: July 17, 2024

Ivermectin is anti-cancer, anti-viral, anti-parasitic and now neuroprotective

Reproduced from original article:
https://expose-news.com/2024/07/10/ivermectin-is-neuroprotective

By on  July 10, 2024

Ivermectin may not just be the anti-parasitic, anti-cancer, anti-viral repurposed drug we recognise but may have multiple other neuroprotective benefits for humanity in an era where we all may be subjected to neurotoxins – some apparent like vaccines and others invisible like electromagnetic frequencies (“EMFs”).

Ivermectin for Parkinson’s Disease – MS, Stroke, Chronic Pain, Anxiety, Depression, and Schizophrenia? Modulated through P2X4 Receptors

By Dr. Justus R. Hope

We all should know that ivermectin is effective not only against river blindness but can be repurposed against many different types of cancer, even against metastatic disease.

During the 2020 pandemic, ivermectin saved many lives worldwide, and not just in the Intensive Care Unit. Ivermectin has also been used to treat long covid and long vaxxed patients by eminent physicians like Dr. Pierre Kory. Some people, like yours truly take ivermectin weekly for its protective or preventative effects.

When you consider the broad spectrum of its anti-disease activity in combination with its vast safety profile, why would you not?

Ivermectin is not only anti-parasitic, but it is anti-viral, anti-bacterial and anti-cancer. But today we know there is more and much more.

Dr. William Makis recently wrote about how ivermectin has properties of promoting remyelination in demyelinating diseases like multiple sclerosis. However, ivermectin has long been known to have potential effectiveness against motor neuron disorders like ALS or Lou Gehrig’s disease.

Ivermectin has shown such great promise against ALS, a patent application was filed by Belgian scientists in 2007.

“Use of ivermectin and derivates thereof for the treatment of amyotrophic lateral sclerosis’ (Publication No.: WO/2008/034202A3), to cover the use of ivermectin and analogues, to prevent, retard and ameliorate a motor neuron disease such as amyotrophic lateral sclerosis and the associated motor neuron degeneration.”

There is emerging evidence that ivermectin may be effective not just against ALS, but against a variety of neurological disorders including Parkinsonism, a disease that many link with the mRNA injections.

Courtesy FLCCC Substack

Ivermectin exerts much of its neuroprotective effects by modulating P2X4.

“Because of its action on P2X4 receptors, ivermectin has potential with respect to preventing alcohol use disorders[92] as well as for motor neuron disease.[93]”

As an aside, ivermectin reverses the effect of alcohol on P2X4 and has the potential to reduce cravings and consumption of alcoholic beverages in those afflicted with substance use disorder.

However, back to neuroprotection.

“Ivermectin (IVM), a positive modulator of P2X4Rs, enhanced levodopa (L-DOPA)-induced motor behaviour. Thus, IVM is increasing striatal dopamine release through enhanced cholinergic activity on dopamine terminals.”

If it is neuroprotective, and the evidence is growing that it is, and humanity is being bombarded with various toxins and electromagnetic frequencies each day that compromise our nervous system, perhaps there is reason to consider ivermectin as a neuro-protective repurposed drug worthy of use during this dangerous time in our history.

Ivermectin’s main mechanism of action in neuroprotection seems to be its stabilisation of P2X4 receptors.

“Ivermectin is a positive allosteric modulator of P2X4 that stabilises this subunit in the open state [20], which consequently may also prevent P2X4 internalisation [21, 22].”

Why is the stabilisation of P2X4 so important?

Because overexpression of P2X4 is not only a disease driver in ALS and Parkinsonism, it plays a key role in many other diseases including Multiple Sclerosis, Alzheimer’s Disease, Chronic Neuropathic Pain, Migraine, Epilepsy, Alcohol Use Disorder, Depression, Bipolar, Schizophrenia and Anxiety.

Or to put it more technically, this study explains the pathological role of P2X4:

“In various pathological states, such as trauma, ischemia, chronic pain, neurodegenerative processes and several neuropsychiatric disorders, de novo expression of P2X4 and/or an increase in cell surface P2X4 density has been reported in microglia and/or neurons, thus suggesting possible key and multiple roles of neuronal and microglial P2X4 receptors in the establishment and/or maintenance of these pathologies [25]. Changes in the intracellular expression of P2X4 may also have important consequences in the pathophysiological context.”

The following study on the effect of allosteric modulators on P2X4 – like ivermectin – highlighted its potential effectiveness in neuroprotection.

“Collectively it appears that there is good evidence that positive allosteric modulation of P2X2, P2X4, and P2X7 receptors may be of therapeutic benefit in a number of different conditions summarised in Figure 2. It is also clear that there may be endogenous molecules, particularly in the central nervous system, that could act as positive modulators to enhance the action of the physiological agonist ATP (e.g., neurosteroids on P2X2 and P2X4).”

Ivermectin may not just be the anti-parasitic, anti-cancer, anti-viral repurposed drug we recognise but may have multiple other neuroprotective benefits for humanity in an era where we all may be subjected to neurotoxins – some apparent, and others invisible like EMF.

About the Author

Justus R. Hope is a writer’s pseudonym for a medical professional and author who has written extensively on the topics of medicine, health and disease. He graduated summa cum laude from Wabash College and earned his medical degree from Baylor College of Medicine. He also completed a residency in Physical Medicine & Rehabilitation at The University of California Irvine Medical Centre. He has practised medicine for over 35 years and maintains a private practice in Northern California.

Dr. Hope has written several books, including ‘Ivermectin for the World’, ‘Surviving Cancer, Covid-19, and Disease: The Repurposed Drug Revolution’ and ‘Ivermectin for Freedom’. His work focuses on the use of repurposed drugs to treat various diseases, including cancer and covid-19.

He publishes articles on a Substack page titled ‘Repurposed Drugs: Powers & Possibilities’ which you can subscribe to and follow HERE.

 

Posted in ALS, Brain, Cancer, Coronavirus, Corruption, Parasites, Parkinson's, Vaccinations | No Comments »

Posted by: | Posted on: October 11, 2023

What Are the Key Micronutrients for Your Brain?


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2023/10/09/brain-nutrients.aspx
The original Mercola article may not remain on the original site, but I will endeavor to keep it on this site as long as I deem it to be appropriate.

Analysis by Dr. Joseph Mercola     Fact Checked     October 09, 2023

brain nutrients

STORY AT-A-GLANCE

  • Micronutrients refer to food-based vitamins and minerals your body requires for optimal functioning. The four primary types are water-soluble vitamins, fat-soluble vitamins, macrominerals and trace minerals
  • Micronutrients catalyze enzymatic processes, have antioxidant activity and modulate your immune system
  • Long-term micronutrient deficiencies can contribute to the development of neurodegenerative processes and neurological diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and amyotrophic lateral sclerosis (ALS)
  • Some of the most important micronutrients involved in Alzheimer’s disease are vitamins A, B, C, D and E, selenium, copper, zinc, iron and manganese. In the case of copper, iron and manganese, elevated levels are typically the problem
  • In the case of Parkinson’s disease, key micronutrients include vitamins A, D, E, B1, B6, B9 and C

Micronutrients refer to food-based vitamins and minerals your body requires for optimal functioning, and even mild deficiencies can contribute to chronic disease. Micronutrients can be divided into four primary types:

  • Water-soluble vitamins such as B vitamins and vitamin C
  • Fat-soluble vitamins such as vitamins A, D, E and K
  • Macrominerals such as calcium, magnesium, sodium and potassium (minerals your body needs in larger amounts)
  • Trace minerals such as iron, zinc, copper and selenium (minerals your body needs in very small amounts)

Micronutrient Deficiencies Can Drive Neurodegeneration

A recent scientific review1,2 published in the peer-reviewed journal Nutrients discusses the role of micronutrients in neurological disorders specifically, noting that long-term deficiencies may be involved in the cause and subsequent development of neurodegenerative processes and neurological diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and amyotrophic lateral sclerosis (ALS).

As noted in this paper, the primary function of micronutrients is their “catalytic effect in enzyme systems, either as cofactors or as components of metalloenzymes.” Other essential roles include antioxidant activity and immune modulation.

When you’re deficient in micronutrients, especially long term, peripheral nerve damage and/or damage to the central nervous system can result, which in turn can contribute to a variety of neurological diseases, including Alzheimer’s and Parkinson’s.

Key Nutrients Involved in Alzheimer’s Disease

While any number of nutrients can impact your risk for Alzheimer’s disease, some of the most important players are vitamins A, B, C, D, and E, selenium, copper, zinc, iron and manganese. In the case of copper, iron and manganese, elevated levels are typically the problem. As explained by the authors:3

“Elevated levels of Hcy [homocysteine] are associated with cognitive impairment. Because of the involvement of vitamins B9, B12, and B6 in Hcy metabolism, hypovitaminosis of these vitamins [i.e., lack of these vitamins] lead to hyperhomocysteinemia [elevated homocysteine].

Substitution of these vitamins helps to decrease the levels of Hcy. However, it has been reported that high doses of vitamins B9, B12, and B6 do not influence the cognition of patients with mild AD [Alzheimer’s disease].

Other vitamins are also associated with AD pathogenesis: thiamine (B1) deficiency has been observed in patients with cognitive impairment, and supplementation improved the symptoms. Vitamin B12 has a direct effect on tau proteins — it inhibits their fibrilization. Vitamin B3 (niacin) may have protective properties against AD and other types of cognitive decline.

Prolonged treatment with vitamin E is in consideration as beneficial in the management of AD, but the outcome is still unclear. Vitamin A inhibits amyloid-β plaque formation.

Vitamin D hypovitaminosis is acknowledged as a risk factor for AD. The pathogenic and therapeutic effects of vitamin D are not yet fully known, but its neuroprotective and anti-inflammatory functions are crucial. It was proposed as a potential therapeutic option for individuals with AD.

Detection of copper can be useful when diagnosing and preventing AD. Significantly higher levels of copper have been found in the brain tissue of AD patients. Copper supports oxidative stress, and it induces neurofibrillary tangle formation by tau hyperphosphorylation.

Another element involved in the pathogenesis of AD is zinc. Low plasmatic levels of zinc are repeatedly associated with decreases in learning ability and memory. Zinc status affects the progression of AD.

The neurotoxicity of manganese can also be associated with AD: it influences the function of astrocytes and the synthesis and degradation of glutamate. Monitoring of manganese can be one of the strategies for preventing AD.

The correlation of higher selenium levels with higher cognitive abilities in the elderly was reported. It is also believed that selenium deficiency may be linked to AD causation. Imbalance in iron metabolism and its accumulation also participates in AD development. One of the proposed novel strategies for Alzheimer’s disease prevention is a diet rich in antioxidants.”

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Important Notes on Iron

Unfortunately, this review does not go into detail about iron. The key issue with iron is you don’t want elevated iron levels. Most adults have excessive iron and do not need more.

Instead, they need to lower their iron, which is easily done by donating blood on a regular basis. What’s more, low ferritin is typically a sign that copper insufficiency is preventing proper iron recycling. In this case, increasing copper will allow the stored iron to recycle, thereby correcting the problem. To learn more about the hazards of high iron and simple ways to screen for and lower it, please see “Why Managing Your Iron Level Is Crucial to Your Health.”

Key Nutrients Involved in Parkinson’s and ALS

In the case of Parkinson’s disease, key micronutrients include:4

Vitamin A
Vitamin D — Has anti-inflammatory effects and lowers oxidative stress. Deficiency is associated with dopaminergic neuronal death. according to the authors, it’s been “proven that adequate vitamin D serum levels might avoid Parkinson’s disease onset and possibly improve clinical outcomes.”

Higher serum concentration of vitamin D has also been shown to improve motor symptoms, and getting at least 15 minutes or more of sunlight exposure per week is associated with a lower risk of Parkinson’s
Vitamin E — Improves the function of the dopaminergic receptors, and higher levels are associated with lower Parkinson’s incidence. Vitamin E-rich diets have been shown to be protective, reducing the risk of Parkinson’s more than carotenoids or vitamin C
Thiamine (B1) — Low thiamine speeds up the degeneration of dopaminergic neurons. Thiamine and folate play important roles in the olfactory system, and many Parkinson’s patients develop impaired taste and smell, which is indicative of a deficiency in one or both of these B vitamins
B6 — Low B6 is a known risk factor for Parkinson’s
Folate (B9) — Elevated homocysteine is a risk factor for Parkinson’s and induces dopaminergic neuron death in Parkinson’s patients. B6, B9 and B12 help keep homocysteine levels in check
Vitamin C — Parkinson’s patients routinely have lower plasma vitamin C levels than healthy controls

The featured paper also reviews the key micronutrients involved in ALS and other motor neuron diseases, myasthenia gravis (an autoimmune disorder affecting the neuromuscular junction), multiple sclerosis (MS), Huntington’s disease (a neurodegenerative disorder resulting in involuntary movements and cognitive impairment), epilepsy, ischemic stroke, myopathy (a muscle disorder), neuropathy, restless leg syndrome and injuries to the central and peripheral nervous systems.

Signs and Symptoms of Nutrient Deficiency

In most cases, symptoms of micronutrient deficiencies do not become apparent until your body is severely depleted, and even then, they can be difficult to identify if there’s no test available.

Oftentimes, symptoms are nonspecific, and include things like frequent infections and skin problems, and as your health deteriorates, more micronutrients are used up, thereby speeding up their depletion. Some micronutrient deficiencies do have more identifiable symptoms, though, such as:

Anemia (iron, copper and/or B12 deficiency) Scurvy (vitamin C)
Osteomalacia or softening of the bones (vitamin D) Pellagra (niacin)
Hemorrhagic diseases (vitamin K) Night blindness (vitamin A)

Your Brain Needs Glucose for Optimal Function

It’s important to recognize that, of all the organs in your body, your brain has the highest energy requirement, and as you age, the mitochondrial genes that drive energy production become less active, leaving your brain more susceptible to disease.5

The mitochondria tend to be less dense and more fragmented, and generate much lower amounts of energy. That does not mean that neurodegeneration is a given, however. You can effectively prevent this fate by eating correctly and having a healthy lifestyle in general.

Free radicals catalyzed by excessive reactive oxygen species (ROS) formed at the level of the mitochondria are typically extremely harmful, and one of the most effective ways to minimize them is to make sure you’re eating enough healthy carbs, such as fruit, because glucose is the optimal fuel for creating energy in your mitochondria.

how do you burn glucose

Your mitochondria can only burn one fuel at a time — either fat or glucose. As illustrated above, fats are broken down in a process called beta oxidation into acetyl-co A, which gets fed into the Krebs cycle. Carbs are broken down to pyruvate, which cannot enter the electron transport chain until they are converted to Acetyl-Co-A by pyruvate dehydrogenase.

The key here is that there’s a stealth switch that controls which of these fuels your mitochondria will burn. The switch has been given the name the Randle Cycle, but it is more helpful to visualize it as a railroad switch that changes the tracks of the train. The train can only travel down one track: not both. This is because only one type of fuel can be burned at a time.

Burning glucose in your mitochondria creates more energy and fewer ROS, raises your metabolic rate, and produces carbon dioxide, which protects against oxidative (reductive) stress and oxygenates cells. All of these things will help protect your brain function.

In a best-case scenario, you will metabolize, or burn, glucose in your mitochondria with minimal reductive stress. When you do this, you will only generate 0.1% ROS.

This route is also incredibly efficient at energy production, creating 36 to 38 adenosine triphosphates (ATP) for every molecule of glucose that is metabolized. However, for this to occur, you need to consume less than 30 to 40% of your calories as fat. When you consume significantly more than that amount, the switch changes to burn fat in your mitochondria and your ability to burn glucose will be impaired.

Chronically oxidizing fats as your primary fuel will also tend to increase your cortisol level, resulting in chronic inflammation, both of which accelerate the aging process.

So, in summary, burning glucose in your mitochondria creates more energy and fewer ROS, and raises your metabolic rate. It also produces carbon dioxide as a byproduct, which protects against oxidative (reductive) stress and oxygenates cells. All these things will help protect your brain function.

For more details about the Randle Cycle and how your metabolism works, see “Crucial Facts About Your Metabolism” and “Crucial Facts About Your Metabolism, Part 2.”

Gut Problems Also Likely Cause of Parkinson’s Disease

A new study6 in the October 2023 issue of Molecular Psychiatry showed that the presence of damaged mitochondrial DNA in the bloodstream is sufficient to cause all symptoms of Parkinson’s disease. The mitochondrial debris is then activated by the endotoxin (lipopolysaccharide) receptor TLR4.

Endotoxin is produced in your gut when you eat fermentable carbs that you are unable to digest in your stomach and small intestine. The carbs then travel to the large intestine, where they fuel the growth of gram-negative bacteria that grow and die. When they die, the endotoxin in their cell wall is released, activating the TLR4 receptor.

The Ray Peat approach is to increase the amount of simple carbs in your diet so your mitochondria can be optimally fueled. But there is strict caution to avoid fermentable carbs for the very reason that they can create endotoxin and activate the TLR4 receptor.

When introducing carbs, it is important to do it slowly, and make sure you are not having digestive symptoms like belching, bloating or gas, which are signs that the carbs aren’t being digested in your upper digestive system. If this is the case, you will need to use small amounts of fruit juices without pulp until your gut can digest the carbs without symptoms.

Lion’s Mane Mushroom May Protect Your Cognitive Function

In addition to basic micronutrients, a number of other supplements can also help protect your cognitive function. One interesting one is lion’s mane mushroom (Hericium erinaceus), which has a long history of use in traditional medicine.

Buddhist monks, for example, traditionally used lion’s mane mushroom tea to enhance brain function and heighten focus. In modern times, several studies have confirmed lion’s mane’s neuroprotective and cognition-enhancing effects, including the following:

A 2023 study7 found that Lion’s mane extract can enhance memory by promoting neuron projections and connections to other neurons.
In a 2020 study,8 patients with mild Alzheimer’s disease who were given three 350-milligram capsules of lion’s mane mushroom per day for 49 weeks improved their cognitive test scores.
An epidemiological study9 published in 2017, which included 13,230 participants 65 years of age and older, found those who ate mushrooms at least once a week had “a lower risk of incident dementia, even after adjustment for possible confounding factors.” The greatest risk reduction was among those ate mushrooms three times or more per week.
A similar but smaller study10 published in 2019 reported that those who ate the most mushrooms had a 43% lower risk of developing mild cognitive impairment, independent of confounding factors such as alcohol consumption, cigarette smoking and high blood pressure.
A 2016 study found extracts from lion’s mane mushroom reduced symptoms of memory loss in mice and prevented neuronal damage caused by amyloid beta plaques known to accumulate in the brain with Alzheimer’s disease.
A 2010 study11 involving seniors between the ages of 70 and 74 found higher intakes of fruits, vegetables, grain products and mushrooms improved cognitive performance.

You can consider adding mushrooms like lion’s mane to your diet as they can be an excellent addition to nearly any meal. They complement all kinds of grass-fed meats and wild-caught fish, go well in nearly any salad and can be added to soups, casseroles and other meals.

However, it is crucial to choose organically grown mushrooms as fungi easily absorb air and soil contaminants. Alternatively, you could opt for an organic supplement or extract.

Posted in ALS, Alzheimer's, Brain, Food, Gut, Minerals, Mitochondria, Nutrition, Parkinson's, Vitamins | One Comment »

Posted by: | Posted on: July 5, 2023

Did Lou Gehrig Die Because of Low Omega-3s?


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2023/07/05/omega-3-and-als-risk.aspx
The original Mercola article may not remain on the original site, but I will endeavor to keep it on this site as long as I deem it to be appropriate.

Analysis by Dr. Joseph Mercola     Fact Checked     July 05, 2023

STORY AT-A-GLANCE

  • A lack of omega-3 fats may have been involved in Lou Gehrig’s death from the disease, as research shows these healthy fats offer protection for ALS patients
  • Higher levels of omega-3 fats, particularly the plant-based omega-3 fat alpha-linolenic acid (ALA), were linked to slowed decline and reduced risk of death in ALA patients
  • The balance of omega-3s you consume is key; since processed foods are loaded with omega-6 fats, it radically skews the omega-3 to omega-6 ratio and inhibits your body’s innate ability to synthesize beneficial EPA and DHA
  • It was 1939 when Gehrig bid farewell to baseball, as his ALS symptoms left his body unable to perform; history shows that our lopsided consumption of ALAs began in the early 1900s, when people were discouraged from eating natural animal fats, leading to increased intake of vegetable oils
  • There are likely a number of contributing factors to ALS, but it’s quite possible that low omega-3 fats were among those that contributed to Gehrig’s case

Amyotrophic lateral sclerosis (ALS) is better known as Lou Gehrig’s disease, named for the beloved New York Yankees baseball player who died of the condition. A number of factors may have played a role in Gehrig’s health decline, including repeated head trauma,1 which is associated with ALS.

A lack of omega-3 fats may have also been involved, however, as research shows these healthy fats offer protection for ALS patients.2 The study, by Harvard researchers, found higher levels of omega-3s led to longer survival and slower functional decline in those with ALS.

However, what this study fails to point out, and that I discuss in my interview with Nils Hoem above, is the fact that reducing seed oil omega-6 in the form of linoleic acid is likely equally important. This is because when your body is loaded with omega-6, the enzymes that convert the omega-3 fat, ALA, are largely used up by the omega-6 fat, LA, and used to make arachidonic acid rather that the important EPA and DHA fats.

Eating Foods High in Omega-3s May Benefit ALS

Omega-3 fats are well-known for their neuroprotective effects, and research published in Neurology3 supports their favorable role in ALS. The study involved 449 people with ALS, whose symptom severity and disease progression were scored and tracked for 18 months. Blood levels of omega-3 fats were also measured, with participants divided into four groups, from lowest to highest.4

Higher levels of omega-3 fats, particularly the plant-based omega-3 fat alpha-linolenic acid (ALA), were linked to slowed decline and reduced risk of death.5 Among those who died during the study, 33% belonged to the group with the lowest levels of ALA, compared to 19% in the highest ALA group.

Even after adjusting for family history, age and other factors, people with the highest ALA levels had a 50% lower risk of death than those with the lowest.6 Eicosapentaenoic acid (EPA), another omega-3 fat that’s found in fatty fish and krill oil, was also associated with lower death risk in the study.7

Lead study author Kjetil Bjornevik, assistant professor of epidemiology and nutrition with Harvard T.H. Chan School of Public Health, explained:8

“Prior findings from our research group have shown that a diet high in ALA and increased blood levels of this fatty acid may decrease the risk of developing ALS. In this study, we found that among people living with ALS, higher blood levels of ALA were also associated with a slower disease progression and a lower risk of death within the study period.

These findings, along with our previous research, suggest that this fatty acid may have neuroprotective effects that could benefit people with ALS.”

The Correct Balance of Omega-3s Is Essential

It’s interesting that this study highlighted ALA, and even stated linoleic acid (LA), a type of omega-6 found in industrially processed seed oils, had a protective effect.9 As explained by Hoem — a research scientist with Aker BioMarine, the largest krill oil company in the world — in the video above, there are two polyunsaturated fats (PUFAs) that are considered essential in conventional medicine.

One of them is LA, which is an 18-carbon molecule. The other is ALA, which also has 18 carbons. Since your body cannot make these fats, you must get them from your diet. That said, since LA is found in nearly every food, and you only need very small amounts, it’s virtually impossible to become deficient in LA. In fact, most people consume far too much LA, as it’s abundantly present in most ultraprocessed foods.

Others, such as the omega-3s EPA and DHA, which have 20 and 22 carbons respectively, can be synthesized in your body, provided you have enough available delta-6-desaturase, an enzyme responsible for their production from ALA.

The problem is that there’s competitive inhibition for that enzyme, so when you have 10-fold (1,000%) more omega-6 in your system, as many people do, then the delta-6-desaturase will be used to convert the omega-6 into arachidonic acid, instead of converting the ALA into EPA.

Since processed foods are loaded with omega-6 fats, it radically skews the omega-3 to omega-6 ratio and inhibits your body’s innate ability to synthesize beneficial EPA and DHA.

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Increasing Omega-3 Is Necessary for Most People

Again, when you have large quantities of LA in your diet, it inhibits the enzyme, delta-6 desaturase, that converts ALA into EPA and then DHA. So, it’s important to lower your LA intake as much as possible so your body can more easily convert any plant-based omega-3, found in flax, hemp and chia seeds, into the animal-based omega-3 fats EPA and DHA.

This competition for delta-6 becomes a moot point if you reduce your LA intake to only 1% to 2% of daily calories. But most people consume 20% to 25% of their calories in the form of LA, which means they have stored up this fat in their cells and it will take up to seven years to get it out.

Restricting LA intake will automatically balance out your omega-3s naturally. But the other alternative is to increase your intake of animal-based omega-3s, which can essentially push the omega-6 out of your membranes. Ideally, you’d do both. According to Hoem:

“The amount of omega-6 is so huge compared with the omega-3s that the only feasible way of increasing your omega-3s in the membranes is through taking omega-3s. Then there is a 1-to-1 exchange of EPA and DHA for omega-6s in the membrane.

So, if you increase one molar amount of EPA and DHA in the membrane, then you kick out exactly the same amount of omega-6. And it’s important to realize that the membrane will be a reflection of your intake of omega-6s versus omega-3s. You can’t really do much with the omega-6s because they’re everywhere, but you can fix it by increasing your intake of long chain omega-3s.”

It was 1939 when Gehrig bid a fond farewell to baseball, as his ALS symptoms left his body unable to perform.10 History shows that our lopsided consumption of ALAs began in the early 1900s, when people were discouraged from eating natural animal fats such as butter and lard.11

This led to a significant increase — more than twofold — in the intake of LA, largely from vegetable oils.12 So, while there are likely a number of contributing factors to ALS,13 it’s quite possible that low omega-3 fats were among those that contributed to Gehrig’s case.

Sports-Related Head Injuries Also Have an Omega-3, ALS Link

Another interesting connection is the many head injuries that Gehrig suffered — and this, too, has an omega-3 connection. Repetitive head injuries can lead to chronic traumatic encephalopathy (CTE),14 which may be associated with development of motor neuron disease.

CTE doesn’t typically occur after one or two concussions. Most individuals affected have had hundreds or thousands of blows to the head, including not only concussions but also many lesser sub-concussive impacts, the latter often being the biggest factor.15 This seems to describe Gehrig. As reported by PBS:16

“Lou Gehrig was called the Iron Horse not only for his incredible strength and speed, but also because he was always in the line-up, no matter what injury he incurred the day before.

On numerous occasions, he was ‘beaned’ by an errant pitch or hit in the face by ground balls, suffered repeated concussions, episodes of loss of consciousness, and other forms of head trauma, without the slightest protection, beyond wearing a woolen baseball cap.

Gehrig collided with rapidly moving objects unrelated to the batter’s box or first base, as well. In 1924, for example, during a post-game fight with the Detroit Tigers, Gehrig took a swing at Ty Cobb, missed, fell, and hit his head on concrete pavement, only to lose consciousness for a brief period of time.”

The omega-3 fat DHA may help for brain trauma, specifically helping the brain resist oxidative stress while preserving membrane homeostasis and function after injury. University of California at Los Angeles researchers suggested that dietary DHA may “counteract broad and fundamental aspects of TBI [traumatic brain injury] pathology that may translate into preserved cognitive capacity.”17

Brain Benefits of Omega-3s Are Well-Established

Omega-3 fats are vital to your brain. A study in the journal Neurology found “older women with the highest levels of omega-3 fats … had better preservation of their brain as they aged than those with the lowest levels, which might mean they would maintain better brain function for an extra year or two.”18

In addition, older adults with memory complaints who consumed DHA, alone or in combination with EPA, had improved memory.19 Low DHA levels have been linked to memory loss and Alzheimer’s disease, and some studies suggest degenerative brain diseases may potentially be reversible with sufficient DHA.20,21

This makes sense, since DHA is an essential structural component of your brain, found in high levels in your neurons, the cells of your central nervous system. When your omega-3 intake is inadequate, your nerve cells become stiff and more prone to inflammation as the missing omega-3 fats are substituted with omega-6 instead.

Once your nerve cells become rigid and inflamed, proper neurotransmission from cell to cell and within cells becomes compromised. You can read more about this in my book, “Superfuel,” cowritten with James DiNicolantonio, Pharm.D. DHA also stimulates the Nrf2 pathway, one of the most important transcription factors that regulates cellular oxidation and reduction, and aids in detoxification.22

Additionally, DHA increases heme oxygenase 1,23 a protein produced in response to oxidative stress, and upregulates antioxidant enzymes — all of which are important for brain health.

Best Sources of Omega-3s

While fish oil is often what comes to mind when considering omega-3 supplementation, it’s not the best option. This is because, in most commercial fish oil supplements, the DHA and EPA are delivered in the form of ethyl esters.

Ethyl esters are essentially a synthetic substrate, created through the micro distillation process of crude fish oil. Most corporations produce ethyl ester fish oil because it’s far less expensive to produce than the triglyceride form. Ethyl esters are also easier to work with during processing, as they have a higher boiling point, which becomes important when the oils are heated and purified of environmental pollutants.

The problem with ethyl esters is they’re the least bioavailable form of omega-3. Free acids of fish oil have an absorption rate of at least 95%. EPA in its natural triglyceride form had a 69% absorption rate in one study, while ethyl ester forms absorbed only about 20% as well as the free acids.24

Importantly, unstable molecules are also more prone to oxidative damage and thus rancidity, which means consuming synthetic fish oil could potentially cause more harm than good.25 Ideally, consume omega-3 fats in whole-food form by eating fatty, cold-water fish.

This includes wild-caught Alaskan salmon, sardines, anchovies, mackerel and herring. If you choose to use a supplement, krill oil provides a superior alternative to fish oil. To ensure you’re getting enough beneficial omega-3 fats, whether you’re getting them from cold-water fish or krill oil, measure your omega-3 index, a measure of the amount of EPA and DHA in the membranes of your red blood cells.

And remember, for optimal health and brain benefits, in addition to increasing EPA and DHA, you’ll absolutely want to radically reduce your intake of LA as low as possible to ensure your omega-3 intake is properly balanced.

You can use Cronometer.com to carefully measure and enter your foods and it will tell you just how much LA you are eating. The goals is under 5 grams, but the lower the better. Mine is about 2.5 grams or about 0.8% of total daily calories. The goal is to get below 2% of daily calories.

Posted in ALS, Oils, Omega-3, Omega-6, Processed Food | One Comment »
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