Part 1 HERE

Now on to the [mostly] human studies –

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Low level laser therapy (LLLT), also known as photobiomodulation, is the use of low-energy red, near-infrared, and infrared light to treat a variety of health conditions like pain and inflammation but it can also be used to improve physical performance. 

Introduction

Essentially, a low-powered laser or light-emitting diode (LED) is used to shine a specific wavelength of light onto the skin of a patient to elicit certain physiological effects in the underlying tissue without causing any damage. Some examples of conditions often treated with LLLT include rheumatoid arthritis, chronic neck and back pain, periodontitis, and muscular injuries.  

The light source may be in the form of a laser or LED and the wavelength of light produced usually falls into the range of 660 nm (red) or 800-900 nm (near-IR/IR) [R, R]. 

Treatment sessions are usually short, lasting only seconds to minutes in duration, and are usually conducted every other day for weeks to months.

Surprisingly, unlike many other treatment modalities used to address similar conditions, there are virtually no reported side effects from LLLT.  

Effects of PBM/LLLT

Inflammation 

One study examined post-injury pain and recovery time in athletes who were treated with an average of four 20-minute sessions of infrared light therapy and compared them to historical values [R]. The average recovery time in athletes treated with LLLT was significantly shorter at 9.6 days when compared to the average anticipated recovery time of 19.2 days. 

A review on muscle repair in animal models concluded red light therapy has the capacity to reduce inflammation, positively impact growth factors, and increase angiogenesis [R]. One animal study showed that LLLT reduced inflammation in an injured muscle [R]. 

A well-known effect of chemotherapy is oral mucositis, which is inflammation that results in the  breaking down of the lining of the mouth. A systematic review concluded LLLT significantly reduced the incidence and severity of chemotherapy-induced oral mucositis [R].  

A study on chemotherapy patients showed a significant reduction in self-reported pain with LLLT [R].

For pain, physical performance, skin & hair and more, head over to Patreon! Five bucks a month for access to this and all previous articles. It’s ad-free and you can cancel if it sucks 🙂

These pork rinds are the bomb. Seriously! And if you like spicy… the former are a little heavier and don’t have a spicy option [yet]

For personalized health consulting services: drlagakos@gmail.com.

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I wrote an article about the human studies with red light therapy / photobiomodulation (PBM) a few years ago and didn’t publish it. I’ll update it and follow-up soon. In the meantime…

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Don’t write off the potential of PBM. We accept many biological influences of light – vitamin D synthesis, circadian rhythms, mood disorders, getting a tan and some endorphins, artificial light and blue blockers – and that’s just the stuff most pertinent to humans.

PBM: what’s it supposed to do?

help with wound healing & pain, inflammation & swelling, although it’s actively being studied in many other contexts – notably, to do with spine/nerves/brain stuff

Some people think it’s important to focus on wavelengths 600-700 nm (for superficial applications) and 780-900 nm (for deeper tissues) and not in between because in part, too much total PBM might reduce efficacy so cut out the ones with less biochemical activity so you can get more of the active wavelengths (Chung, Hamblin et al., 2012).

Disclaimer: there are a lot of inconsistencies in the PBM literature. Different doses, duration, surface area exposed, etc., etc., that make it hard to come to firm conclusions on any of it. That, plus, some of the units can get pretty pricy, especially since there’s no clear guarantee they’ll do anything for you. I feel ya.

One effect that seems pretty consistent is on improving skin health/appearance.

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These pork rinds are the bomb 🙂

For personalized health consulting services: drlagakos@gmail.com.

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At first, this article reads like a sarcastic blog post or something (Kalantar-Zadeh et al., 2019).

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[their words in italics; my commentary is not]

How often have you been told to eat more protein and less carbohydrates to stay healthy?

Uhmmm, never?

This is not an emerging food culture but rather a prevailing dogma in our society.

What society is that?!

Physicians, dietitians and other health care professionals tell us constantly about the advantages of a high-protein diet (HPD), such as losing weight rapidly, burning calories, diminishing appetite, preventing obesity, managing metabolic syndrome and treating diabetes. 

Which physicians!

This contemporary creed has gone so far that we feel continuously pressured to eat more protein and less carbohydrates, including even less fruits and vegetables. 

Am I taking crazy pills?

We feel compelled to eat only the meat patty of the sandwich and leave behind the bun when eating in front of others, otherwise we may lose credibility among friends and peers. 

Yes, crazy pills.

If somebody dares to recommend a ‘low-protein diet’ (LPD) or, even worse, to imply that ‘HPD may cause harm’, then it would be considered a serious aberration to health and a taboo.

This is some seriously emotionally charged stuff. TABOO! And as I read on, it became clear…….

For the rest of this article and more, head over to Patreon! Five bucks a month for access to this and all previous articles. It’s ad-free and you can cancel if it sucks 🙂

These pork rinds are the bomb 🙂

For personalized health consulting services: drlagakos@gmail.com.

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or, the biggest mouse study that’s ever been done (Hu, Speakman, et al., 2019)

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Background rant: 20 years ago I thought I had a firm understanding of CIM. 10 years ago things got a little dicey here and there. Since then, the goalposts have been shifted so far and so frequently it’s a mess… we’ve come a long way from Atkins (for better or worse)

I disavow.

That said, regardless of where the goalposts were set, everyone should bookmark this study. They varied every macronutrient in nearly every possible way and took a variety of metabolic assessments (insulin sensitivity, body weight, food intake, etc.).

So whether or not their study tested the CIM to which you subscribe, there is still a ton of information here. My comments are mainly on CIM here lol

Speakman’s CIM is broken down into 5 somewhat overlapping parts.

1. Increased dietary carbs increases fasting insulin which decreases fasting glucose

-In the context of any CIM, the postprandial state seems more relevant here; as in, ‘carbs increase insulin which reduces glucose and you get fat storage from the insulin and hangry from the hypo.’

These pork rinds are the bomb 🙂

2. Carbs and insulin induce de novo lipogenesis which makes you fat

-My only qualms here are: DNL is quantitatively more of a liver thing, and anyway, most of the fat that gets stored came straight from the diet, not DNL.

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Ultraviolet radiation suppresses obesity and symptoms of metabolic syndrome independently of vitamin D in mice fed a high-fat diet (Geldenhuys et al., 2014)

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Sunlight > vitamin D supps. It is known.

Brief review of vitamin D synthesis: TEAMWORK!

In brief: cholesterol -> 7-dehydrocholesterol in skin; sunlight (UV radiation) converts that into D3 which goes to liver on DBP and is made into 25(OH)-D3. That then goes to kidneys and is transformed into the active form, 1,25(OH)2-D3. What’s not shown in that graphic is when you have enough D, it’s instead converted into an inactive 24,25(OH)2-D3. This prevents toxicity from sunlight D.

Hypervitaminosis D (from supps) is rare but unpleasant.

Seasonally, in some extreme latitudes, fancy UV lamps &/or [speculatively] much cheaper reptile bulbs may supplement sunlight. And it’s not just vitamin D!

This study showed sunlight also increases nitric oxide in the skin, which has effects beyond the D… may also be supplemented with NO-inducing skin creams (also speculative), if applied to the right spots…

Big tie-in with our beloved brown adipose tissue.

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A lot of cool studies about brown adipose tissue (BAT) lately; here’s the rundown.

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More and more, with more sophisticated techniques, scientists are discovering we have more BAT than previously believed. And they all have theories on how it works and if it can be manipulated to make us healthier.

Activated BAT secretes a lot of stuff:

Exercise increases circulating 12,13-diHOME in humans (old, young, male, female, sedentary, active) (Stanford et al., 2018).

In mice, too, and surgical removal of BAT abolishes this effect. Dosing them with 12,13-diHOME increases fatty acid uptake and oxidation in skeletal muscle.

BOOM

Cold exposure induces the enzyme 12-LOX in BAT which synthesizes lipid mediators that improve glucose tolerance (Leiria et al., 2019).

Cold exposure in this #context is a few degrees above your shivering threshold. It’s NOT an ice bath — it’s shorts & a t-shirt in 50(ish) degrees F (10 C).

The good news: if you dislike exercise or find cold exposure unpleasant, there are other ways, eg, beta-3 adrenergic receptor agonism and some nutrients that can be obtained via diet.

For the rest of this article and more, head over to Patreon! Five bucks a month for access to this and all previous articles. It’s ad-free and you can cancel if it sucks 

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An update on brain fatty acid metabolism (Romano et al., 2017)

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This was an interesting review, although it got off to a rocky start by stating: “glucose is the preferred energy substrate of the brain.”

My opinion is that “preferred energy substrate” is a weird concept in this context. When glucose declines and ketones increase, ketones will be used. Are they preferred now?

I’m not saying either are preferred. Just making note of this.

Given the title of the article, I was expecting a lot on DHA/fish oils but there was a good deal on ketones.

Yes, the brain definitely uses ketones; this is particularly important during starvation and it comes in handy during hypoglycemia.

it’s likely that you can avoid going into a coma during hypoglycemia if there are a lot of ketones around. Brain doesn’t use a lot of fatty acids, probably, to reduce the risk of hypoxia and/or oxidative stress (the former because FA oxidation is slow).

-> exercise is probably the number one “anti-aging” agent (good for everything but cognitive health in particular)

-> exercise & ketones -> +brain-derived neurotrophic factor (BDNF)

^^^I rather like BDNF and humbly suggest this may lean toward ketones being more “preferred”

Coconut oil may be helpful in this context.

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Interesting lipid findings from the DELISH study (Mason et al., 2019).

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The nefarious “sdLDL” — whether you’re a believer or not in any cholesterol hypothesis relating to health, most agree that if LDL levels predict disease, it’s the small dense ones that do it best.

DELISH was a good study. Not a super-intensive double-blind randomized crossover study of keto vs. SAD, but rather a moderately ketogenic (> 0.3 mM bHB), “cut out the sugar & processed foods” intervention.

It worked.

The participants cut their carb intake in half but maintained baseline fibre intake suggesting indeed, they were cutting out processed carbs, not non-starchy ones, green leafys, berries, etc.

In the intro, it is mentioned that sometimes, LDL-C increases on a ketogenic diet. This has more to do with the specific foods than the macro’s or process of ketogenesis, and that was a general theme of this paper.

Indeed, this one had to do with red meat…. ooooohhh

If you’re interested to see how it played out, head over to Patreon! Five bucks a month for access to this and all previous articles. It’s ad-free and you can cancel if it sucks 

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Two studies. one compared 6 vs. 3 meals per day (Jakubowicz et al., 2019); the other 6 vs. 2 (Kahleova et al., 2014).

BOTH eTRF!!!!! Finally.

Tl;dr #1: with regard to body composition, 3 protein-containing meals/d seems to be the sweet spot. Muscle likes frequent feedings, but no additional benefit is seen beyond 3x/d.

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Tl;dr #2: If you’re gonna IF, the totality of evidence favors some manner of eTRF.

According to the data, the traditional 3 meal/d eTRF is great, less hunger, more satiating, etc. Or is you want to be like some anti-aging guru and skip dinner a few times/wk & go to bed hungry for that hormetic response or something, there are data supporting that too.

Let’s dive in it -> head over to Patreon! Join the community for up-to-date information about a variety of topics in the health & optimizing wellness space. Five bucks a month for access to this and all previous articles. It’s ad-free and you can cancel if it sucks 🙂

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Many camps here! This is getting fun 🙂

Two different supplements: nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN). Both backed by good science & scientists (one camp is shilling a supplement while the other camp is selling books, which I don’t really care about) (the social media war is, however, hilarious).

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Both precursors appear equally effective in the rodent studies and I expect this to cross over when NMN finally has human studies.

BIG difference that nobody is really talking about is TISSUE SPECIFICITY.

1st problem: commentators were talking about NR/NMN as if it passed from your gullet directly to the liver. NR would be absorbed directly; NMN would be dephosphorylated to NR, absorbed, get re-phosphorylated back to NMN then converted to NAD+.

[insert Slc12a8 image here]

Since NMN and NR cost the same, this doesn’t really matter. Right?

Supp manufacturers just thought that since NMN was one step closer to NAD+, it might make a better precursor. But if it’s converted to NR prior to absorption, who cares?

And if the liver just releases niacinamide (NAM) to the rest of the body, WHO CARES?

THE PLOT THICKENS

This becomes relevant with all the different preparations on the market — intranasal, sublingual, regular oral (NR/NMN), NAD+ directly, and why can’t I just save a ton of money and use NAM instead! Relevant, yes. And interesting. I’ll summarize…

Have you tried any of these? Let us know in the comments 🙂

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