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If Dr. Ken Berry actually meant to say that you need to eat saturated fat for your nerves and brain, he flunks Biochem 101. First of all, your body can make all the saturated fat you need out of carbs and proteins. You don’t need to eat ANY saturated fat. Second, the most common fatty acid in your brain is the polyunsaturated fatty acid (PUFA) called DHA, which you DO need to eat, because you can’t make it from non-fats (you need to eat it or EPA in things like seafood, or at least the precursor omega-3 PUFA called ALA in cold-climate plants.) Ironically enough, ALA is common in Canola oil, which Dr. Berry deprecates, but not in the tropical plant oils that he likes. More on that later.

A diet with a lot of saturated fat is NOT the best for the heart. The American Heart Association continues to recommend low saturated fat diets (with the missing sat-fat replaced by mono and polyunsaturated fat, not by carbohydrates) because the evidence from animal and human trials and even properly controlled epidemiology, shows these the best diets (see reference below—an extensive review of meta analyses [1]). Examples are the DASH hypertension diet and the closely-related Mediterranean diet (which has lots of olive oil for monounsaturated fatty acid, and seafood for DHA). If Dr. Berry thinks he has something better than the Mediterranean diet for longevity, what is his direct evidence?

Saturated fat, of course, is used by the body to make cholesterol (you don’t need to eat any cholesterol for this reason), and it does raise cholesterol levels and it does increase atherosclerosis in nearly every controlled prospective experimental model in animals and humans. This is the gold standard of evidence in medicine.

One can go only so far with epidemiology, because occasionally when one bad thing (saturated fat) is heavily replaced for calories by another bad thing (certain carbohydrates) one detects no epidemiologic effect from changing just the first thing.

That happens with various high and low saturated fat diets around the world enough to make saturated fat look benign as a single input variable. It is not. Rather, what these studies really show is that replacing butter with sugar or high glycemic carbs gives you a diet equally bad for the arteries. One cannot see how bad that is, until one compares these with low-carbohydrate, low-saturated-fat diets, which are less common, but better. The double-negative tradeoff of carbs and saturated fats (where carbs are a statistical “confounder”) is one of those occasional cruel misdirectional things that happen with imperfectly controlled past-observations, but (again) it’s why biomedical knowledge consists of more than just epidemiology.

The saturated oils Dr. Berry recommends are by themselves on the edge of PUFA deficiency. This can be dramatic: for example the only way I know to give dogs atherosclerosis nutritionally, is to feed them just coconut oil for fat, and NO monounsaturates or PUFA. Apparently a little PUFA is extremely important for the heart, and larger amounts do no harm. There are hints that high PUFA diets are risks for certain cancers, but that merely underscores the need to get monounsaturates like olive and Canola where one can, and some PUFA foods. I know of no civilization that eats a lot of coconut oil that doesn’t eat seafood as well, so that combination is safe.

Canola oil is merely rapeseed oil bred to remove erucic acid and other potential toxins. It is high in monounsaturates and ALA and of all the plant oils is probably closest to optimal for human nutrition. Olive oil is probably better than Canola for frying, since ALA will oxidize, but Canola’s ALA is very important for vegans who need an omega-3 PUFA plant oil to convert to brain DHA. Seafood and olive oil are a fine replacement for Canola, but the person who cannot eat meat or seafood had better look for a baking and salad oil with ALA in it, and Canola oil is the best for this. Linseed oil is hard to digest and hard to work with, so that leaves Canola as the best omega-3 alternative for vegans. Dr. Berry never mentions his problem with Canola beyond saying it is GMO. But he is wrong there, as it doesn’t have to be. Canola as a product (1970’s) was created with hybrid not GMO techniques, and although GMO Canolas exist now, there also exist certified non-GMO and “organic” Canola oils which are labeled with a butterfly and tested to make sure no GMO Canola has crept in (there are tests available for this too complicated to go into here, but you can be sure).

In short, the ONLY part of Dr. Berry’s piece I agree with is dumping your hydrogenated shortening products (Crisco, etc.) in the garbage. That’s why I give this segment a D, rather than the F it otherwise deserves.

Steven B. Harris, M.D.

[1]

Cardiovascular disease (CVD) is the leading global cause of death, accounting for 17.3 million deaths per year. Preventive treatment that reduces CVD by even a small percentage can substantially reduce, nationally and globally, the number of people who develop CVD and the costs of caring for them. This American Heart Association presidential advisory on dietary fats and CVD reviews and discusses the scientific evidence, including the most recent studies, on the effects of dietary saturated fat intake and its replacement by other types of fats and carbohydrates on CVD. In summary, randomized controlled trials that lowered intake of dietary saturated fat and replaced it with polyunsaturated vegetable oil reduced CVD by ≈30%, similar to the reduction achieved by statin treatment. Prospective observational studies in many populations showed that lower intake of saturated fat coupled with higher intake of polyunsaturated and monounsaturated fat is associated with lower rates of CVD and of other major causes of death and all-cause mortality. In contrast, replacement of saturated fat with mostly refined carbohydrates and sugars is not associated with lower rates of CVD and did not reduce CVD in clinical trials. Replacement of saturated with unsaturated fats lowers low-density lipoprotein cholesterol, a cause of atherosclerosis, linking biological evidence with incidence of CVD in populations and in clinical trials. Taking into consideration the totality of the scientific evidence, satisfying rigorous criteria for causality, we conclude strongly that lowering intake of saturated fat and replacing it with unsaturated fats, especially polyunsaturated fats, will lower the incidence of CVD. This recommended shift from saturated to unsaturated fats should occur simultaneously in an overall healthful dietary pattern such as DASH (Dietary Approaches to Stop Hypertension) or the Mediterranean diet as emphasized by the 2013 American Heart Association/American College of Cardiology lifestyle guidelines and the 2015 to 2020 Dietary Guidelines for Americans.

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If Dr. Ken Berry actually meant to say that you need to eat saturated fat for your nerves and brain, he flunks Biochem 101. First of all, your body can make all the saturated fat you need out of carbs and proteins. You don’t need to eat ANY saturated fat. Second, the most common fatty acid in your brain is the polyunsaturated fatty acid (PUFA) called DHA, which you DO need to eat, because you can’t make it from non-fats (you need to eat it in things like seafood, or at least the precursor omega-3 PUFA called ALA in cold-climate plants.) Ironically enough ALAis common in Canola oil, which Dr. Berry deprecates, but not in the tropical plant oils he likes. More on that later. A diet with a lot of saturated fat is NOT the best for the heart. The American Heart Association continues to recommend low saturated fat diets (with the missing sat-fat replaced by mono and polyunsaturated fat, not by carbohydrates) because the evidence from animal and human trials and even properly controlled epidemiology, shows these the best diets (see reference below–an extensive review of meta analyses [1]). Examples are the DASH hypertension diet and the closely-related Mediterranean diet (which has lots of olive oil for monounsaturated fatty acid, and seafood for DHA). If Dr. Berrythinks he has something better than the Mediterranean diet for longevity, what is his direct evidence? Saturated fat, of course, is used by the body to make cholesterol (you don’t need to eat any cholesterol for this reason), and it does raise cholesterol levels and it does increase atherosclerosis in nearly every controlled prospective experimental model in animals and humans. This is the gold standard of evidence in medicine.

One can go only so far with epidemiology, because occasionally when one bad thing (saturated fat) is heavily replaced for calories by another bad thing (certain carbohydrates) one detects no epidemiologic effect from changing just the first thing.

That happens with various high and low saturated fat diets around the world enough to make saturated fat look benign as a single input variable. It is not. Rather, what these studies really show is that replacing butter with sugar or high glycemic carbs gives you a diet equally bad for the arteries. One cannot see how bad that is, until one compares these with low-carbohydrate, low-saturated-fat diets, which are less common, but better. The double-negative tradeoff of carbs and saturated fats (where carbs are a statistical “confounder”) is one of those occasional cruel misdirectional things that happen with imperfectly controlled past-observations, but (again) it’s why biomedical knowledge consists of more than just epidemiology. The saturated oils Dr. Berryrecommends are by themselves on the edge of PUFA deficiency. This can be dramatic: for example the only way I know to give dogs atherosclerosis nutritionally, is to feed them just coconut oil for fat, and NO monounsaturates or PUFA. Apparently a little PUFA is extremely important for the heart, and larger amounts do no harm. There are hints that high PUFA diets are risks for certain cancers, but that merely underscores the need to get monounsaturates like olive and Canola where one can, and some PUFA foods. I know of no civilization that eats a lot of coconut oil that doesn’t eat seafood as well, so that combination is safe. Canola oil is merely rapeseed oil bred to remove erucic acid and other potential toxins. It is high in monounsaturates and ALAand of all the plant oils is probably closest to optimal for human nutrition. Olive oil is probably better than Canola for frying, since ALAwill oxidize, but Canola’s ALA is very important for vegans who need an omega-3 PUFA plant oil to convert to brain DHA. Seafood and olive oil are a fine replacement for Canola, but the person who cannot eat meat or seafood had better look for a baking and salad oil with ALA in it, and Canola oil is the best for this. Linseed oil is hard to digest and hard to work with, so that leaves Canola as the best omega-3 alternative for vegans. Dr. Berry never mentions his problem with Canola beyond saying it is GMO. But he is wrong there, as it doesn’t have to be. Canola as a product (1970’s) was created with hybrid not GMO techniques, and although GMO Canolas exist now, there also exist certified non-GMO and “organic” Canola oils which are labeled with a butterfly and tested to make sure no GMO Canola has crept in (there are tests available for this too complicated to go into here, but you can be sure).

In short, the ONLY part of Dr. Berry’s piece I agree with is dumping your hydrogenated shortening products (Crisco, etc.) in the garbage. That’s why I give this segment a D, rather than the F it otherwise deserves.

Steven B. Harris, M.D.

[1] https://www.ahajournals.org/doi/epub/10.1161/CIR.

Advertising can really mislead you when it comes to your health. Thinking a certain cooking oil is good for you can ruin the quality of your dinner, and harm your health.

Huge corporations farm huge GMO crops, then highly process the seeds to get “vegetable oils”. After spending all the money to do this, they have to convince you the oil is healthy so you will buy it.

Your health is too important to buy this crap from big-food, and the silly recommendations from big-medicine. Here is a list of the oils you Should use to cook with, and a list of the ones you should avoid. And, I’ll also tell you the one you should get out of your house right now.

What other LIES have you been told? ➡ https://amzn.to/2FYIAj8

—Join me and let’s optimize your health! –

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The 2 Gig service is targeting households with heavy internet users who are now forced to work from home due to COVID-19. “So we’re more than a little excited to announce 2 Gig today—bringing even more bandwidth and speed to customers in internet-intensive households who may need more than a gig to do their thing, whatever that may be,” wrote Amalia O’Sullivan, Google Fiber’s director of product management, in the announcement. (That said, upload speeds will remain at 1Gbps.)

Google Fiber is currently looking for subscribers in Nashville, Tennessee, and Huntsville, Alabama, to sign up as testers for the 2 Gig service. The beta will then roll out to other Google Fiber cities in the fall before the official launch. Interested customers can also go to the Google Fiber website to sign up for email updates on the 2Gbps service’s availability.

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We should save their DNA and resurrect them or keep in a bubble environment.

Close To Home

The researchers behind the study warned that each time an animal goes extinct, it also threatens humanity’s continued survival.

“The current extinction crisis is one of the more urgent global environmental problems and the only one [that is] truly irreversible,” study author Gerardo Ceballos of the National Autonomous University of Mexico’s Institute of Ecology told Earther. “Once a species is gone, there is no way to bring it back. Our paper indicates that is vastly speeding up.”

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Modifications to chromosomes in “engram” neurons control the encoding and retrieval of memories.

When the brain forms a memory of a new experience, neurons called engram cells encode the details of the memory and are later reactivated whenever we recall it. A new MIT study reveals that this process is controlled by large-scale remodeling of cells’ chromatin.

This remodeling, which allows specific genes involved in storing memories to become more active, takes place in multiple stages spread out over several days. Changes to the density and arrangement of chromatin, a highly compressed structure consisting of DNA and proteins called histones, can control how active specific genes are within a given cell.

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Analysis revealed that variants in the HMGCR gene region, which represent proxies for statin treatment, were associated with overall cancer risk, suggesting that statins could lower overall cancer risk.

Cholesterol-lowering drugs called statins may reduce cancer risk in humans through a pathway unrelated to cholesterol, says a study published today in eLife.

Statins reduce levels of LDL-cholesterol, the so-called ‘bad’ cholesterol, by inhibiting an enzyme called HMG-CoA-reductase (HMGCR). Clinical trials have previously demonstrated convincing evidence that statins reduce the risk of heart attacks and other cardiovascular diseases. But evidence for the potential effect of statins to reduce the risk of is less clear.

“Previous laboratory studies have suggested that lipids including cholesterol play a role in the development of cancer, and that statins inhibit cancer development,” explains lead author Paul Carter, Cardiology Academic Clinical Fellow at the Department of Health and Primary Care, University of Cambridge, UK. “However, no trials have been designed to assess the role of statins for in clinical practice. We decided to assess the potential effect of therapy on cancer risk using evidence from human genetics.”

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When it comes to vitamin D, most adults exhibit either frank deficiency, which results in clear clinical symptoms, or insufficiency, which often goes undetected. But how that insufficiency impacts physical health and the vulnerability of older adults to frailty as they age has been difficult to determine.

Now a University at Buffalo study of 24–28–month-old mice, the equivalent of 65-to-80-year-old adults, has found that can be slowed with what might be considered “over” supplementation with vitamin D, referred to as “hypersufficiency.”

Published Sept. 30 in Nutrients, the research builds on previous work that Kenneth L. Seldeen, Ph.D., first author and research assistant professor in the Department of Medicine in the Jacobs School of Medicine and Biomedical Sciences at UB, has been conducting for more than a decade with colleague Bruce R. Troen, MD, professor of medicine and chief of the Division of Geriatrics and Palliative Medicine and director of the Center for Successful Aging, both in the Jacobs School.

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Gets advanced, but some might like.

A research team from Cologne has discovered that a change in the DNA structure—more precisely in the chromatin—plays a decisive role in the recovery phase after DNA damage. The key is a double occupation by two methyl groups on the DNA packaging protein histone H3 (H3K4me2). The discovery was made by scientists under the direction of Prof. Björn Schumacher of the Cluster of Excellence for Aging Research CECAD, the Center for Molecular Medicine Cologne (CMMC), and the Institute for Genome Stability in Aging and Disease at the University of Cologne. The specific change enables genes to be reactivated and proteins to be produced after damage: The cells regain their balance and the organism recovers. The protective role of H3K4me2 was identified in experiments with the nematode Caenorhabditis elegans. The study has now been published in the journal Nature Structural & Molecular Biology.

The genome in every human cell is damaged on a daily basis, for example in the skin by UV radiation from the sun. Damage to the DNA causes diseases such as cancer, influences development, and accelerates aging. Congenital malfunctions in DNA repair can lead to extremely accelerated aging in rare hereditary diseases. Therefore, preservation and reconstruction processes are particularly important to ensure development and to maintain tissue function. DNA, which is rolled up on packaging proteins—the histones—like on cable drums, is regulated by methyl groups. Various proteins are responsible for placing methyl groups on histones or removing them. The number of groups on the packaging proteins affects the activity of genes and thus the production of the cell.

In experiments with the nematode, the research team showed that after repairing damaged DNA, two methyl groups were increasingly found on the DNA packages. Furthermore, they found that errors in placing these two methyl groups on the histones (H3K4me2) accelerated the damage-induced aging process, while increased position of this histone alteration prolongs the lifespan after DNA damage. By controlling the proteins that either set or remove these methyl groups, the resistance to DNA damage—and thus the aging process of the animals—could be influenced.

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A research collaboration between Kumamoto University and Nagasaki University in Japan has found that components leaking from broken muscle fibers activate “satellite” muscle stem cells. While attempting to identify the proteins that activate satellite cells, they found that metabolic enzymes, such as GAPDH, rapidly activated dormant satellite cells and accelerated muscle injury regeneration. This is a highly rational and efficient regeneration mechanism in which the damaged muscle itself activates the satellite cells that begin the regeneration process.

Skeletal is made up of bundles of contracting muscle fibers and each is surrounded by —muscle stem cells that can produce new muscle fibers. Thanks to the work of these cells, muscle fibers can be regenerated even after being bruised or torn during intense exercise. Satellite cells also play essential roles in muscle growth during developmental stages and muscle hypertrophy during strength training. However, in refractory muscle diseases like and age-related muscular fragility (sarcopenia), the number and function of satellite cells decreases. It is therefore important to understand the regulatory mechanism of satellite cells in muscle regeneration therapy.

In mature skeletal muscle, satellite cells are usually present in a dormant state. Upon stimulation after muscle injury, satellite cells are rapidly activated and proliferate repeatedly. During the subsequent myogenesis, they differentiate and regenerate muscle fibers by fusing with existing muscle fibers or with together. Of these three steps (satellite cell activation, proliferation, and muscle differentiation), little is known about how the first step, activation, is induced.

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August was the second-highest month for sales ever.

Colorado has seen over $1.1 billion in marijuana sales since the COVID-19 pandemic began in this country, according to figures from the state Department of Revenue.

Legal marijuana sales topped $200 million in August for the second month in a row, reaching the second-highest monthly total since recreational sales started in 2014. Counting back to March of this year, when Colorado and the rest of the nation began shutting down over the pandemic, dispensaries have sold over $1.1 billion in marijuana products — and that’s not counting sales in September and October.

Dispensaries sold over $218.6 million worth of marijuana products in August, DOR data shows. Recreational sales accounted for more than $176.5 million (also the second-highest monthly total since 2014), while medical marijuana sales remained strong at just over $42 million.

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