Dr. Rhonda Patrick on DHA in Phospholipid Form and the Prevention of Alzheimers | Hacker News Reader

Dr. Rhonda Patrick on DHA in Phospholipid Form and the Prevention of Alzheimers

zenpatient.com

141 pointsdtawfik138 comments

Rhonda Patrick is one of my favorite people to listen to. She did a great interview with Joe Rogan talking all about health, digestion, nutrients, diets, etc.

https://www.youtube.com/watch?v=9M8X_bs_fzI

Her podcast has been a great source of interviews with interesting researchers. Her guest appearances have also been great (she's been on Peter Attia's podcast).

Here are some great notes from her talk with Peter Attia: https://podcastnotes.org/2018/07/03/attia-patrick/

(Disclosure, I'm part of the podcastnotes team)

Let me add two interviews with Tim Ferriss:

Dr. Rhonda Patrick on Life Extension, Performance, and Much More https://tim.blog/2014/06/10/the-tim-ferriss-show-rhonda-patr...

Exploring Smart Drugs, Fasting, and Fat Loss https://tim.blog/2017/05/04/smart-drugs-fasting-and-fat-loss...

The paper is open access, so the full text is available sans paywall. :) Worth checking out if for no other reason than to appreciate the figures! https://www.fasebj.org/doi/10.1096/fj.201801412R

If APOE4 combined with reduced DHA impairs glucose transport into the brain, would increasing blood ketone levels help sidestep this issue (along with increasing dietary DHA of course)?

How do you think algal oil would work out? Also, are you interested in studying groups of peoples and cultures and determining if e.g. somebody who's lived a life on the Mediterranean diet is better adapted to this kind of uptake and if that's reflective of a decline in AD for that group? Or maybe even just better overall mental health?

When you eat oily fish you are eating the same oil that is expelled and inserted into a capsule. So how is the form changed?

This is a type of fish oil that usually comes from krill. It has a higher capacity to pass the blood-brain barrier of carriers of the APOE4 gene.

The natural oil in the fish is found as triglycerides and as phospholipids.

A triglyceride is an ester made from three fatty acid molecules attached to a glyerol molecule (you get esters by reacting carboxylic acids with alcohols, and glycerol is a polyol alcohol with three hydroxyl groups). A phospholipid is very similar except one of the fatty acids is replaced by some hydrophilic molecule that's attached to the glycerol via a phosphate group.

The problem from a commercial point of view is that the fatty acids are mixed, but fish oil is only sold by EPA/DHA concentration. Nobody will buy natural fish oil because the EPA/DHA levels are too low. The solution is transesterification, where the glycerols are removed and replaced with ethanol. Ethanol is an alcohol with only a single hydroxyl group, so it can only form an ester with a single fatty acid. Now that all the fatty acids are in separate molecules, you can distill off the lower boiling ethyl esters of short chain fatty acids. EPA and DHA are long chain fatty acids, so their higher boiling ethyl esters will be left behind.

Theoretically could transesterify the ethyl esters back to triglycerides again, but when you can just sell the ethyl esters as "fish oil concentrate" there's no reason to.

This is an excellent, concise, clear explanation, thank you.

> fish oil is only sold by EPA/DHA concentration. Nobody will buy natural fish oil because the EPA/DHA levels are too low.

So only free fatty acids are allowed to be listed on the label as EPA/DHA? They're not allowed to count any esterified fatty acids?

I don't know the details of labeling laws, but I believe fish oil is most commonly sold as ethyl esters, and this is called "fish oil concentrate". Free fatty acids are considered a defect in edible oils. They taste rancid and make the oil decay faster. Triglycerides and ethyl esters both get digested in the small intestine by pancreatic lipase enzymes, releasing free fatty acids where you can't taste them. Both raise blood levels of free fatty acids, and the quantity of ethanol released from the ethyl esters is small enough that I think it's very unlikely to matter.

But as the article points out, phospolipids get digested differently, and phospolipids are converted to ethyl esters in the transesterification processing too. By focusing only on blood levels of fatty acids, people overlooked a potentially important difference between natural and processed fish oil.

Is this the same for bottled flax oil? I am under the impression that flax oil has similar properties to fish oil.

I've never heard of concentrated flax oil, and all flax oil I've seen has the ALA levels I'd expect of natural flax oil. However, as discussed elsewhere in the comments, humans are not good at converting ALA to EPA and DHA, so flax oil cannot be considered a full substitute for fish oil.

Chelation. When you concentrate the oil you can remove impurities there are a lot of in fish. In particular, Mercury and I think Cadmium too impede and reverse myelination, making taking fish oil for the nervous system benefits almost counterproductive.

But eg sardines should not contain much of any heavy metal? Salmon is also pretty low in mercury.

Is there any actual clear link between dietary DHA and serum DHA? I’m guessing no.

Humans survive on quite a wide range of dietary fat sources and composition. I stopped supplementing with fish oil after realizing there’s lots of “science” and few facts.

There has to be, since humans can't make it themselves. (Assuming that's true.)

They can.

> This finding suggests that when animal foods are wholly excluded from the diet, the endogenous production of EPA and DHA results in low but stable plasma concentrations of these fatty acids.

https://www.ncbi.nlm.nih.gov/pubmed/16087975

TIL. Thank you.

And yet in the article,

> Unfortunately, the body cannot produce DHA on its own, and it must be acquired through the diet.

So is Rhonda waaaaay behind the times re: that 14-year old paper? Or are the levels described in that paper negligible? Or did I misinterpret something, or what?

Good question. She may be simplifying things, or not thinking of vegans/vegetarians. No doubt it's a suboptimal amount.

Fish is not the only source of DHA. Walnuts, acai berry and flaxseeds are also good sources.

The only good vegetable source of DHA is some types of algae. The foods you listed contain alpha-linolenic acid, which the human body can convert to EPA and then to DHA, but this is an inefficient process and might not always meet the full requirements for those longer chain omega-3 fatty acids. See:

https://rnd.edpsciences.org/articles/rnd/pdf/2005/05/r5505.p...

More bluntly, ALA supplementation doesn't work:

https://www.ncbi.nlm.nih.gov/pubmed/19269799?dopt=Abstract

Walnuts also have a lot of Omega 6 which will lessen the conversion of Omega 3 into useable forms.

Do I understand this correctly that if I consume a lot of Omega 6 (I love olive oil and nuts and consume large quantities of both) I might actually harm myself? Do I make Alzheimer disease more likely by Omega 6 rich diet?

EDIT: I confused Omega 3 <> Omega 6, corrected.

They aren't. In order to overcome the omega-6 metabolic preference, you need to consume, at a minimum twice as much omega-3 oils as omega-6, but actually closer to 4x.

Twice as much omega-3 means eliminating olive oil, soy, most nuts, and many other foods. Or, alternatively, downing a pint or so of flax seed every day.

Everything you said is true except I can't see how fish helps in this case. You still need to eat a lot of fish (especially since most fish are very low fat, salmon is a good choice) and cut Omega 6 sources, if you want to make Omega 3:Omega 6 ratio 2:1.

Algae, and the fish that live on it, don't provide omega-3 oils. They provide the fully formed end products, DHA and EPA, so the metabolic bottleneck is avoided.

Not sure why this is getting downvoted, it's a valid concern.

Going by this review, I would say that supplementation does work:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176556/

Yes, there is. I have had mine tested as I altered my diet to include more fish roe, fish liver, and fatty fish. I took my omega6:omega3 ratio from 3.5:1 to 1.5:1 in ~3 months.

Total O3: 10.2% -> 16.5%

DPA: 1.2% -> 3.2%

EPA: 3.4% -> 4.3%

DHA: 5.4% -> 9.2%

I don't have a "before" on the standard american diet, but IIRC the average american has an omega6:3 ratio of about 15-20:1.

Serum levels could mean your body has more DHA than it needs, without an established level at which some kind of deficiency develops.

I’m not trying to prove a point except this: People who have no regard to dietary DHA and consume no fish don’t exhibit any of the problems claimed in articles and by nutritionists. I’ve been vegan for 20 years for example and my skin is fine, I don’t supplement DHA, I don’t have dementia or other health problems.

This contrasts pretty strongly with homocysteine/B12 deficiency or iron deficiency. There’s no good evidence that a clinical syndrome of DHA deficiency even exists. Whenever I dig into studies serum levels are all over the place.

There’s quite a lot to be suspect of here. The conclusions drawn from our limited understanding of fatty acid metabolism just doesn’t match reality.

FWIW, these were not serum levels, this was RBC (red blood cell).

> I have had mine tested as I altered my diet...

How/where did you get tested?

I got it done via OmegaQuant, costs $99 and can be ordered online.

Dr. Patrick- if DHA/EPA is re- esterized, as it is in Biotest’s Flameout supplement. Does this re-esterization put it in a phospholipid form to be absorbed thru the BBB?

Fish Heads Fish Heads rolley polley fish heads

Fish heads Fish heads eat them up... YUM!

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