High intensity deliberate practice that you can only do for short amounts of time per session
How is that different from flow work?
CasioTheSane
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I’m not sure if you’ve read Mihály Csíkszentmihályi or not, but he argued that flow states are more likely when a task is more complex/challenging, and the person has a high level of appropriate skill that makes it possible (with substantial effort) to complete the task.
For me this often occurs while programming, sailing, or doing math- especially if I need to solve a new problem with those skills that will be especially challenging.
Once I’m in ‘flow’ it is a distinct mental experience—I am totally into it and lose any sense of time passing, or of needing to motivate myself until I am interrupted either by my own body, or by something external.
Cal Newport in Deep Work (his own word for flow work) defines “Deep Work” as anything that requires skills that would take at least a year to develop if a person was already generally educated, smart, and motivated.
I stopped using pomodoros for flow-work, because it would break my flow state. I’ve found roughly 2 hour chunks work better for flow, without any particular warning to stop me if I feel like going longer. If I am in flow, I want it to keep going as long as possible, until I am fatigued, or the problem is solved.
But I would have thought that if there was widespread ‘central hypothyroidism’, someone would have twigged by now, since that form does show up if you do a full panel of hormone tests
Which tests? I am not aware of any simple blood test that measures the endpoint of thyroid activity on metabolic rate (except, arguably, cholesterol levels), rather than just the state of the T4->TRH->TSH->T4 feedback loop.
mostly T4 with a bit of extra T3′, but no-one has particularly clear ideas on what works and what doesn’t or why
The challenge with T3 is it has a very short half-life, one would need to take very small doses impracticably often to achieve stable levels. Taking mostly T4 with a bit of T3 helps compensate for the reduction in T3 production due to feedback without the problems caused by trying to obtain nearly all T3 directly from a supplement.
Thanks for the reference to Ray Peat, I hadn’t heard of him before. Can you link to the best expression of his thoughts?
His own essays at raypeat.com are the only accurate source, but can be challenging to read. Most of the summaries you will find online don’t do him justice.
he was basically making his patients hyperthyroid
Why is this a reason not to reject it? He is essentially arguing that the major cause of cardiovascular disease is population-wide high rates of hypothyroidism. It would be a circular argument to dismiss that because his treatment leads to a greater than average metabolic rate. One would also need evidence of a disadvantage that outweighs the advantages. His patients seemed to be doing well, or at least he doesn’t report them exhibiting any classic signs of hyperthyroidism. He was primarily adjusting dose based on body temperature to the upper end of the normal non-hyperthyroid range.
to help them lose weight
I have seen studies on thyroid supplementation as a weight loss strategy, and it causes loss of lean tissue (muscle, etc.) more than fat.
You wouldn’t need to invoke the idea of ‘hormone resistance’ because TSH and T4 tests normally used to diagnose hypothyroidism don’t measure the active hormone—T3. T4 is just a prohormone with very little direct activity on metabolic rate.
In primates, metabolism is regulated primarily in the liver by T4->T3 conversion, so if this is inhibited for any reason it will suppress metabolism without showing up on those tests. Low calorie intake, and poor nutrition are known to cause this (e.g. Euthyroid sick syndrome). In cases of poor liver conversion, supplementing T4 can actually make symptoms worse, as it will further suppress metabolism by lowering the small amount of T3 production from the thyroid (via the TSH feedback loop).
I assume you have heard of Ray Peat? I personally had good luck applying his ideas to increase my energy levels, and my pulse, body temperature, and cold tolerance raised as well—without supplementing thyroid. His general idea is pretty simple- just look at what conditions and nutrients maximize T4->T3 conversion, and provide them (low stress, high nutrient diet).
Broda Barnes work is very interesting. It blows my mind that he published a paper in The Lancet showing that desiccated thyroid lowered cholesterol levels and seemed to prevent cardiovascular disease in his patients, and that it remains virtually un-discussed and uncited (http://www.ncbi.nlm.nih.gov/pubmed/13796871).
You’re right, we do understand the pathophysiology of many diseases, and those are the ones that have been mostly eradicated. The major chronic diseases that remain are very poorly understood such as type II diabetes, cancer, cardiovascular disease, and alzheimer’s.
I spend a lot of time reading about ‘alternative’ ideas about these diseases, and many seem promising, but aren’t taken seriously by the mainstream. It’s definitely possible that they’re ignored for a good reason, but I haven’t been able to find the reasons yet. This is the biggest problem I’ve found with trying to be ‘critical of everything.’ In very few instances do I find myself quickly understanding and agreeing with the mainstream view. Instead, the more I read the more my opinion seems to diverge from the mainstream view. I have made an effort to discuss these issues personally with specialized experts, so they could help point out factors I may be missing, or not understanding correctly. I am a PhD candidate in the life sciences, so I have the opportunity to meet with research professors at my university in person to help clarify my understanding.
Here are two example theories, regarding cancer and cardiovascular disease in particular.
1) The idea that cancer isn’t initiated by genetic mutations, but that mutations are a downstream phenomena that results after damage to the mitochondria occurs.
This stems from the initial observation by Warburg, that lack of control over glycolysis is part of the cancer cell phenotype. This phenotype can be triggered by a large number of factors which inhibit mitochondrial respiration including hypoxia. Later it was found that the mitochondria in cancer cells undergo a phenotypic change, where the cristae structure is lost. Nuclear transfer experiments have shown that a ‘mutated’ cancer nucleus placed into a healthy cell cytoplasm does not exhibit a heritable cancer phenotype. Conversely, a healthy nucleus placed into a cancerous cell cytoplasm does exhibit a heritable cancer phenotype.
Here is a review article covering the evidence for this hypothesis:
Cancer as a metabolic disease: implications for novel therapeutics http://carcin.oxfordjournals.org/content/35/3/515
More evidence for this hypothesis includes the observation that active thyroid hormone levels (T3) are inversely correlated with cancer mortality rates in the general population. T3 is a key regulator of mitochondrial respiration:
Thyroid hormones and mortality risk in euthyroid individuals: The Kangbuk Samsung Health Study. http://www.ncbi.nlm.nih.gov/pubmed/24708095
2) The finding that treatment for hypothyroidism drops cholesterol levels significantly, and virtually abolishes cardiovascular disease without the side effects seen from statins. The late Broda O. Barnes was an experimental endocrinologist and a clinical doctor, and he extensively documented this phenomena in his books and publications.
The idea here is that the central mechanism of cardiovascular disese is a low metabolism which inhibits cholesterol clearance from the blood via reduced steroid hormone synthesis, and reduced bile synthesis. The pathophysiology of cardiovascular disease begins with a long residence time of cholesterol particles in the blood, resulting in their oxidation. This can be reversed by any strategy that restores a normal (higher) metabolic rate: a carefully designed diet and/or thyroid hormone supplementation.
Here is a good introduction to this idea:
The Central Role of Thyroid Hormone in Governing LDL Receptor Activity and the Risk of Heart Disease http://blog.cholesterol-and-health.com/2011/08/central-role-of-thyroid-hormone-in.html
I am not insisting that these ideas are correct, or are some sort of ‘well proven answer’ to these diseases. I’m just pointing out that they seem promising, but are relatively ignored. If they prove accurate, much of the mainstream research on these phenomena would seem to be barking up the wrong tree.
You might notice that both of these examples are essentially the same theory. This is an appealing concept to me: most age-related chronic diseases may be centered around a common process of age related impaired mitochondrial function and/or improper hormonal regulation of mitochondrial function. Insufficient chemical energy (ATP) to fuel normal biological function would have widespread consequences, and could present as a diverse array of seemingly disconnected symptoms. I’ll admit, this sounds somewhat like a modern molecular version of vitalism. However, unlike vitalism it makes specific testable predictions, and involves a very specific mechanism. It’s also consistent with the ‘free radical’ and ‘tissue peroxidizability index’ theories of aging, which involve (among other things) progressive oxidative damage of unsaturated fats (such as cardiolipin) in the mitochondrial inner membrane.
I have been attempting to do this with biology and medicine, seriously for about 5 years now. Not by actually repeating experiments, but in trying to understand the original evidence, and see if I agree that it was interpreted correctly. Of course this is nearly impossible as biology is too broad and complex for one person to understand all of the details.
It’s a confusing mess, but I think I am still learning a lot. Even if I come to agree with most of the mainstream ideas, I’d like to think I’d then understand them more deeply, in a way that is more functionally useful.
For much of medicine, there really isn’t any biological basis or evidence to review. Much of modern medicine involves covering up symptoms with drugs proven to do this, without understanding the underlying cause of the symptom.
Excellent post, thanks for putting so much work into a clear explanation. I will re-investigate Ling’s work more carefully, and also see if I can find the mistakes in his thermodynamics calculations you mention. I have been biased towards his work and not looking critically enough, because it seems to explain some surprising observations about drug activity I’ve found in my own research- but that’s no excuse.
I am interested in the possibility that Ling could be entirely wrong about membrane physiology, but this gel phase shift phenomena could still be important in the cell. If Ling and Pollack are wrong about long distance effects from protein surfaces, that might not destroy their arguments as the cytosol is very dense, and the distance between proteins is very short. Albert Szent-Györgyi also did some work on this idea that is very different from Ling’s.
One of my committee members works on physics simulations of protein hydration shells, and I am going to meet with him and see what he thinks about this. The simulations I have seen don’t show significant water structuring, as the water molecules have too much thermal energy.
That’s a good point about intelligence, the way I used that word without defining it in this article is sloppy.
I am interested in the ability to solve important problems. Maybe instead I should talk about something more easily definable such as mental endurance, or limiting the stress response from focused work? Personally, I think if I could work longer in one sitting on a hard problem without stress or fatigue, that alone would count as “increased intelligence” for practical purposes.
I think there are links between the stress response and nutrient availability. In lab mice anyway, sugar seems to reduce stress hormone production during stressful situations. However in practice this might be harmful to doing focused work, if stress improves focus.
Thanks for pointing out the issue of brain energy consumption vs mental activity. I think this entire article hinges on the (unfounded?) assumption that the two are strongly correlated. I am confused about this, and need to learn more about it. I see many articles and researchers claim massive increases in energy consumption with hard mental activity, and others that claim there is none which seems very strange. How are they measuring this? I wonder if people under general anesthesia have much lower, or about the same energy requirements as an awake person?
I need to learn more about this, I don’t have a strong belief. If I understand correctly, this is basically the idea behind the free radical theory of aging (FRTA). One interesting variant of that idea is in the article I linked above, which suggests that the focus should be on “mitochondrial membrane peroxidizability index” rather than antioxidant activity or free radical production.
It seems weird that sugar seems to cause problems in certain populations of people, but not others.
There can be damage or defects in the mitochondria that inhibit it’s ability to respond to hormones, for example per-oxidation of cardiolipin. Cells don’t always die when they have a mitochondrial defect. An extreme example is cancer, where there is major damage to the mitochondria, but the cells continue to live via anaerobic fermentation (aka the Warburg Effect).
Some review articles that talk about these theories:
Cancer as a metabolic disease: implications for novel therapeutics
Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals
Role of cardiolipin peroxidation and Ca2+ in mitochondrial dysfunction and disease
Perhaps sugar and glucose only cause problems in those who can’t metabolize it effectively, for other reasons (or when consumed in excess of your capacity to metabolize them). I used to think high glucose intake caused metabolic syndrome but I can’t reconcile that with the existence of large groups of people (Kitavans, fruitarianism, etc.) that have very high carb diets and don’t develop metabolic syndrome.
In mice, high sugar diets don’t cause metabolic problems or liver damage unless also coupled with high polyunsaturated fat intake. Populations of people with high carbohydrate diets and no metabolic syndrome seem to have very low polyunsaturated fat intake. Could carb restriction protect against the symptoms of metabolic disease, without addressing the underlying cause?
Fructose seems to increase T3 production in the liver, which could be a mechanism behind the sugar high. I am not sure if this is “good” or “bad.”
If you have time to provide links, I would like to read the research you mention- especially on the thermodynamics of ATP and calcium-triggered membrane vesicle fusion. Ling’s work is all very old and doesn’t address any newer research, but Pollack addresses some of the issues you raise in his books. Pollack does love to speculate a lot, but he appears to be careful in distinguishing this speculation from things that have more evidence. Here is also a newer review paper that discusses this and some other ideas related to the role of entropy in biochemistry: Coherent Behavior and the Bound State of Water and K+ Imply Another Model of Bioenergetics: Negative Entropy Instead of High-energy Bonds
I think this would be difficult to observe, because starvation also increases stress hormones which increase motivation. For the most part, brain metabolism remains high in starvation, but other glucose using systems are reduced, to preserve glucose for the brain. Ketones are also used to reduce glucose demands while keeping brain metabolism high. Ancedotally, I seem to be more motivated when fasting or dieting, but more creative when eating a nutritious diet.
Metabolic syndrome, and hypothyroidism (both diseases of decreased cellular energy production) are correlated with reduced intelligence.
Citations:
Pre-morbid intelligence, the metabolic syndrome and mortality: the Vietnam Experience Study.
Contribution of Metabolic Syndrome Components to Cognition in Older Individuals
Cognitive function in non-demented older adults with hypothyroidism.
That’s a good point. I think some old hot water heaters might even be so full of small particles that they’re hard to drain from the bottom, and you might need to get the water from the top.
However, I think most of the sediment would be insoluble in water, and can be avoided by letting the water settle for a few minutes. Any soluble particles would have long since dissolved, sitting in a bath of hot flowing water for years.
Great post.
For food, I think dehydrated potatoes are a particularly effective emergency food. They’re more complete nutritionally than grains and will keep you performing longer in a tough situation.
I also like to store enough fuel to safely get to a friend or family members house in another town, if necessary. My vehicle is diesel, so storing the fuel is somewhat safer than storing gasoline.
Books can be helpful as well- especially easy to read field references for emergency medicine and survival techniques. In my opinion a good book on first aid is more important than an actual first aid kit.
Also, a hot water heater is a giant tank of drinkable water, and is always full. It can be drained from a spigot at the bottom.
However, I don’t really have a strategy to seek out some similar mentors and worry that in engineering it’s a lot more likely to find method-oriented persons. I’m wondering if you have any advice on this.
No, I’m not even sure how to easily tell if someone is method or problem oriented without at least meeting them and talking to them. If you find any ideas on this please share them with me.
intractability of the problems that grabbed my attention in the first place (intelligence amplification/cognition)
That is a very hard problem. This is wild speculation but have you looked at the concept of hormesis? Maybe it’s possible to engineer the right conditions under which the brain improves it’s abilities on it’s own. I think in some cases living organisms can be considered ‘functional systems’ which adapt as much as possible to maintain function in the face of a stress or challenge. This adaptation is limited in part by overall stress levels, and metabolic rate/energy availability. Focused strategies to overcome these limitations may increase adaptive ability. This may require developing a deeper understanding of both stress and metabolism.
Consider a weight lifter that can lift over 1,000lbs, something with probably no evolutionary precedent. They get this way with a combination of very low overall stress, a high nutrient diet that raises the metabolic rate and overall energy availability, a progressively increasing and highly specific stressor, and long rest periods. Perhaps a similar approach could be applied to ‘train’ improved cognitive abilities? One obvious difference is that our brain is limited in size, so there may be tradeoffs involved when we improve one specific skill or ability. I imagine this idea would sound very naive to neuroscientists.
What kind of paradigm shifts do you think will occur for biology in the future?
I can’t predict the future, but this is a fun question good for more wild speculation. I think genetics will be seen as increasingly less significant, and heritable traits and information will be found encoded in many different molecules and structures in living cells.
I also think progressively impaired energy availability (impaired oxidative metabolism) will be viewed as a central phenomena occurring in most degenerative diseases, aging, and failure to adapt to stressors. This simple paradigm will help focus research to understand, fix, and prevent the underlying problems, enabling a shift away from medicine focused on managing symptoms. This is a popular concept in many old medicine systems (such as chinese medicine) but it has limited effectiveness without a deep understanding of the underlying molecular mechanisms, and how to manipulate them.
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Growing crops for biofuel cannot produce more carbon than it consumes over long time scales, because the only source of carbon available to the system is the carbon in the atmosphere. If they are saying biofuels aren’t carbon neutral over long time scales, where is this extra unlimited supply of carbon coming from?