Disclaimer: I’m meat-cancer agnostic. *IF* meat causes cancer (and I don’t think it does), it happens extremely slowly and only at very high levels of intake: to get statistically significant risk ratios, researchers usually look to top vs. bottom quartiles, which is quite a large difference in intake.
Meat-cancer studies Tl;dr: some studies show positive associations, some neutral, and none are negative (ie, it’s unlikely meat prevents cancer).
That said, if meat does cause cancer, here is how it might happen:
1. The “Maybes:” AGEs, leucine/mTOR, methionine, etc., but only in combination with numbers 2 & 3. Not by themselves.
3. Most animal foods have a lot of linoleate 18:2n6 or at least a lot more n6 than n3 (grass-fed is usually a little better in this context). More on this below.
It started out as “lose weight without hunger on LCHF” and went all the way to “effortless fasting on keto.” Works for some and it might be true, but the same can be said for low fat diets! The key, I think, in both contexts, is simple: fewer processed & refined foods… something the Paleo movement got right, imo (although I still think many low-calorie sweeteners are way less unhealthy than HFCS & sugar).
The logic:
1) add “good calories” like almonds to your diet and appetite spontaneously compensates by eating less other stuff: energy neutral
2) you don’t compensate for added “bad calories” like sugar-sweetened beverages: positive energy balance
3) remove bad calories from your diet and you don’t compensate by eating more other stuff: negative energy balance
Humans are incredible omnivorous beasts that can thrive on a great variety of diets, but crumble if you mess with their sleep.
Circadian arrhythmia is thought to be a driving force behind a few types of cancer. But how, exactly, does seemingly harmless things like artificial light, skipping breakfast, or jet lag actually promote tumorigenesis? There are many potential mechanisms, and I’d bet different circadian disruptions promote different cancers in different #contexts.
In some cell types, circadian disruptions which dampen amplitude increase proliferation. This has led to some researchers to believe a robust circadian rhythm per se is tumor-suppressive. In agreement with this, many tumor suppressors are direct targets of circadian transcription factors. As was observed in some skin cancers, you may want suppressed proliferation at some times of the day but not others, so the tissue can renew properly. But you don’t want, for example, skin cells to be proliferating while they’re being exposed to UV light, so this process happens at night (in circadian fashion).
Circadian transcription factors also directly interact with endogenous antioxidant systems.
Cancer clocks out for lunch: disruption of circadian rhythm and metabolic oscillation in cancer (Altman, 2016)
Disclaimer: I’m pro-LC (P<0.05), but not anti-LF because LF works better than LC for some people. And with the exception of things like keto for neurological issues, I think macros take a back seat to many other factors.
Myths: carbs cause insulin resistance (IR), diabetes, and metabolic syndrome. Carbs are intrinsically pathogenic. If a healthy person eats carbs, eventually they’ll get sick.
And the only prescription is more keto.
And of course all of this could’ve been prevented if they keto’d from the get-go.
Proponents of these myths are referring to regular food carbs, not limited to things like Oreo Coolattas (which would be more acceptable, imo). Taubes, Lustig, Attia, and many others have backed away from their anti-carb positions, yet the new brigade proceeds and has even upped the ante to include starvation. Because “LC = effortless fasting?”
Does this sound sane?
“No carbs ever,
no food often…
otherwise diabetes.”
no one in their right mind would say lentils & beans cause diabetes
Over the course of human evolution, diets varied widely over time, seasons, geography, etc., ie, we can obviously thrive on many different dietary patterns… but the light/dark cycle was there the entire time. Why is this not the most important talking/debating point? Why do people think humans need one particular diet but can ignore circadian rhythms?
Because everyone’s still fussing about carbz and what we are “designed to eat”
Quotes are mainly taken from the text. I’ve tracked down some of the cites; the rest are in the back of the book, albeit somewhat unorganized :/
Part 1. We naturally have a cortisol spike first thing in the morning, known as the Cortisol Awakening Response (CAR). This peak, which can be screwed up by artificial light at night or a big evening dinner, helps support morning light-induced dopamine.
Dopamine is great, but may induce impulsivity if it’s unfettered.
Enter: the protein-rich breakfast. It provides tryptophan and a bit of insulin to promote serotonin synthesis (eg, Manjarrez-Gutierrez et al., 1999).
Not enough serotonin to make you crazy, just enough to balance the dopamine = impulse control.
side note: please consider the modern views of Taubes, Lustig, Gardner, Attia, and others on Carbs™. They’re less “Carbs-cause-obesity, keto-for-all, etc.,” and more thinking it might not be Carbs™ per se, but rather processed and refined foods. And #context… And I tend to agree at the moment (nuances and caveats are subject to change, as more evidence accumulates).
disclaimer: I haven’t seen the full text of Hall’s recent study, but that’s not really relevant to what I want to discuss. In other words, I don’t think the full text will provide any additional details on this particular point.
Tl;dr: this study was not designed to prove or disprove metabolic advantage or the insulin-obesity hypothesis.
It’s in the study design: four weeks of low fat followed by four weeks of low carb. We KNOW that weight loss slows over time (especially if calories are controlled, as they were in this study). It has to do with the order of treatments.
I’m totally cool with keto, honestly! but still don’t really like seeing stuff like the above graphic and people interpreting it to mean “KETO IS MUSCLE-SPARING.”
I came across a recent study on a mouse model of Angelman Syndrome (an epigenetic disorder), and wasn’t surprised to learn there’s a strong circadian component to it. Epigenetics are one of the main ways circadian rhythms are programmed.
In this case, the circadian connection is more direct.
Angelman Syndrome (AS): you inherit 2 pairs of each gene, one from Mom and one from Dad. In some cases, one of the copies is silenced via epigenetics and you’re basically just hoping the other one is in good shape. In the genetically relevant region in AS, the paternal copy is silenced and the maternal copy does all the heavy lifting, but in AS, the maternal copy is mutated or absent, so none of the genes in this region are expressed.
Interestingly, scientists found that one of the genes, Ube3a (an ubiquitin ligase), is involved in regulating Bmal1, a core circadian gene (Shi et al., 2015) . And mice with a silenced paternal Ube3a and mutant maternal Ube3a exhibit many of the same circadian symptoms of children with AS. They don’t mimic all of the symptoms as there are many other genes in this region. But both show circadian abnormalities.
Prader-Willi Syndrome (PWS) is the epigenetic opposite: same region of DNA, but silenced maternal copy and mutant or absent paternal copy. This disorder is characterized by massive obesity and low muscle mass (among other things).
While reading about this disorder, I was taken aback with how the obesity was explained.
“Insatiable appetite” (Laurance et al., 1981), although from what I can gather, these children would develop massive obesity even if they were fed cardboard. Some studies even showed no change in food intake and/or energy expenditure (eg, Schoeller et al., 1988), which led some researchers to publish entire papers about how these children must be lying and/or stealing food (eg, Page et al., 1983) .
Further, other researchers even explained their obesity was due to an inability to vomit (Butler et al., 2007).
THEY’RE OBESE BECAUSE THEY’RE NOT BULEMIC.
AYFKM?
When these kids gain weight, it’s nearly all fat mass; when they lose weight, it’s nearly all muscle [shoulda been a BIG hint]… this even led some researchers (who detected no change in fat mass after significant weight loss) to conclude that their techniques to assess body composition must not be valid in this population because: surely, they must’ve lost some fat mass like normal people do.
THEY FAILED TO CONSIDER THIS IS AN EXTREME CIRCADIAN MISMATCH DISORDER IN NUTRIENT PARTITIONING
It was actually painful to read: these kids are being accused of stealing food and not vomiting because that’s the only way to explain it.
NO IT’S NOT, SCIENCE.
They can be forced into losing fat while maintaining some muscle with an extreme protein-sparing modified fast (eg, Bistrian et al., 1977)…
A few research groups have considered the possibility it’s a hormonal disorder, and some fairly long-term studies with GH replacement have shown promising results (eg, Carrel et al., 1999).
Prader-Willi Food Pyramid. Wait, wut? O_o
Some have even speculated involvement of leptin (eg, Cento et al., 1999), although this hasn’t been followed-up on.
Disclaimer: I don’t know the cure or best treatment modality for Prader-Willi, although given the strong circadian component in its sister condition, Angelman’s Syndrome, I strongly believe this avenue should be explored (in combination with the seemingly necessary hormonal corrections, which have been the only successful interventions yet). “Diet” doesn’t work; these kids aren’t obese because they’re stealing food or failing to vomit. Interventions strictly targeting CICO have massively failed this population.
Side note: in the Angelman Syndrome mouse model, *unsilencing* the paternal copy worked… maybe the same could work in PWS (and/or other forms of obesity)…?
Evidence supporting potential circadian-related treatment modalities for PWS:
A Prader-Willi locus IncRNA cloud modulates diurnal genes and energy expenditure (Powell et al., 2013)
Magel2, a Prader-Willi syndrome candidate gene, modulates the activities of circadian rhythm proteins in cultured cells (Devos et al., 2011)
Circadian fluctuation of plasma melatonin in Prader-Willi’s syndrome and obesity (Willig et al., 1986)
And the connection with LIGHT:
Artificial light at night: melatonin as a mediator between the environment and the epigenome (Haim and Zubidat, 2015)
Circadian behavior is light re-programmed by plastic DNA methylation (Azzi et al., 2014)
PWS is much worse than just nutrient partitioning (seriously, just spend a few minutes on any Prader-Willi support forum or this; maybe it is an appetite disorder, but given the data on weight gain [mostly fat mass] and weight loss [mostly muscle mass], it seems far more likely a circadian disorder of nutrient partitioning),
but that component jumped out at me; more specifically, despite the only positive results coming from non-dietary interventions, researchers were still all “#CICO.”
“Lean meat, sugar-free Jello, and skim milk”
FFS
Circadian biology, hormone replacement [where appropriate], and figure out if any specific diets help. PMSF/CR doesn’t work unless “refrigerators and cabinet pantries are locked shut.”
Maybe this applies to other forms of obesity, too.
Maybe.
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secretion happens at night (or at least that’s when it’s supposed to happen):
(an epigenetic disorder), and wasn’t surprised to learn there’s a strong circadian component to it. Epigenetics are one of the main ways circadian rhythms are programmed.
(PWS) is the epigenetic opposite: same region of DNA, but silenced maternal copy and mutant or absent paternal copy. This disorder is characterized by massive obesity and low muscle mass (among other things).
