Posts made by war4512

@war4512 https://www.youtube.com/watch?v=rKr9gjTgCbc&ab_channel=IvanCarsten-Topic

One of the most dopaminergic songs in history.

@Insomniac said in Tracking down the mysterious cause of Dr. Paul Saladino's shockingly rapid aging:

Not a single forehead wrinkle

What implies the lack of wrinkles in Haidut is low inflammation combined with a high level of subcutaneous fat. The fat fills the voids caused by aging. In thin individuals, age-related wrinkles tend to be excessively pronounced.

@Insomniac said in Tracking down the mysterious cause of Dr. Paul Saladino's shockingly rapid aging:

too much sugar

There is no evidence whatsoever to suggest that sugar (sucrose) or other carbohydrates cause accelerated aging.

@Insomniac High protein diet.

@zaaku said in How did you treat your NAFLD and how long did it take?:

Is this recommendation from personal experimentation or from a study? If it's from a study, could you please share it? I couldn't find it.

https://chrismasterjohnphd.substack.com/p/does-choline-deficiency-contribute

@zaaku said in How did you treat your NAFLD and how long did it take?:

In my understanding from reading Peat's work and some papers T3 is helpful in energizing the liver. Did you mean T4?

Reply

At low glucose levels, T3 shifts its metabolic effects, promoting catabolic processes. T3 increases glucose utilization, which can result in chronically low glucose levels, leading to the suppression of glycogen synthase expression.

Low glucose levels, in turn, lead to elevated glucagon levels.

Low blood glucose is a precursor to a stress response, further amplified by neurotransmitters and stress hormones.

Compensatory intake of more carbohydrates throughout the day can be highly beneficial, provided that the root cause of all problems is not excessive neurochemical signaling; treating this process will require time.

@the-MOUSE It depends on the case. In general, it's better not to consume more than 5g of PUFAs per day. If someone were to follow the proposed paradigm while supplementing with algal oil, I don't see a problem. DHA and EPA are better than linoleic acid and gamma-linolenic acid, not to mention osbond or arachidonic acid, because they are precursors to less harmful eicosanoids. DHA and EPA supplementation can be useful, but it really depends on the individual case. I believe that milk fat from grass-fed cows can provide the necessary amounts of DHA through alpha-linolenic acid.

@zaaku said in How did you treat your NAFLD and how long did it take?:

Triglycerides: 48mg/dL
Cholesterol, Total: 184mg/dL
Cholesterol, HDL: 68mg/dL
Cholesterol, LDL: 107mg/dL
TSH: 0.05µIU/mL (Used to be 2.3 before thyroid supp)
ALT: 27U/L
AST: 34U/L
GGT: 52U/L
Albumin: 5.06g/dL

Well, it’s likely that your NAFLD is already in an early stage. Continue with a high-carbohydrate diet—your very good triglyceride levels suggest a state of carbosis (preferential and highly efficient carbohydrate metabolism). The area for improvement is definitely excess weight, which you can reduce with an appropriate calorie deficit, leading to a genuine regression of NAFLD.

@zaaku said in How did you treat your NAFLD and how long did it take?:

Overall I feel significantly better than I used to and I think treating liver + glycogen storage is the final step for me. Sleep is deep and sound, though I wake up once in the middle to replenish sugar. Digestion is smooth with 1 BM per day (sometimes 2). I'm calm and patient and at peace pretty much all the time though I avoid excursions or putting myself in challenging situations because I know I become hypoglycemic. Even the daily walk with my dog leads to a little hypoglycemia midway through so sometimes I want to, sadly, cut it short.

Hypoglycemia, simply put, is a stress response. If possible, perform an OGTT (Oral Glucose Tolerance Test) and consider testing C-peptide levels to assess insulin secretion. To improve glycogen storage, you can supplement with creatine and more carefully control selenium intake by increasing the amount of seafood in your diet, especially those rich in copper.

During a walk or any other physical activity, try to consume easily digestible carbohydrates to prevent a stress response.

I also recommend Masterjohn's article. A very valuable tip.

https://chrismasterjohnphd.substack.com/p/start-here-for-fatty-liver-disease-0a3

@the_black_jew You are obsessed with me.

Ingredients (for about 6 pancakes):

• 1 cup chestnut flour (approx. 120g)
• 15g dark cocoa powder
• 1 egg
• 1 cup skimmed milk
• 30g honey
• A pinch of salt to taste (I use potassium salt, 70/30%)
• 1 teaspoon coconut oil for frying

Preparation:

Sift the chestnut flour and salt into a bowl. Gradually pour in the milk, whisking the batter continuously.
Add the egg, cocoa powder, and honey, mixing until fully combined. The batter should be relatively thick.
Heat a frying pan and grease it lightly with coconut oil. Use a ladle to pour the batter onto the pan, spreading it into a pancake.
Cook the pancakes for a short time, about 1–2 minutes on medium-high heat, until set.

Serve with traditional Italian-style date-coffee spread:

• 6 fresh Medjool dates (about 150g, pitted)
• If using dried dates, soak them in warm water for 10–15 minutes to soften.
• 1 shot of espresso (approx. 40 ml)
• 1/2 americano (approx. 75 ml) – made with espresso + 35 ml water

Preparation:

Let the brewed coffee cool slightly.
Place the dates in a blender, pour in the coffee, and blend into a smooth paste.
Serve the pancakes with the date-coffee spread.
Optional Beverage:
Accompany the meal with coffee mixed with 20g of gelatin.

Nutritional Values:

If the recipe yields approximately 6 pancakes, the nutritional values per pancake are:

• Energy: ~137.5 kcal
• Protein: ~4.3 g
• Fat: ~2.6 g
• Carbohydrates: ~23.6 g

Adding 40g of date spread per serving contributes:

• Energy: ~112 kcal
• Protein: ~0.9 g
• Fat: ~0 g
• Carbohydrates: ~29 g

Overall Nutrition Cronometer Profile for the Meal:

@gg12 said in "Orthorexic Sequence" – My Personal Experience with OCD:

I suffer with OCD as well. I know part of it is physiological but part of it seems to fall in m own hands with how I react to my thoughts. I have let my OCD grow in the unconscious for far too long and have had manic states lately. I am surrounded b people in poor health. My family just follows the massmedias agenda eating PUFA getting shots etc. I try to stay healthy but the food supply is so poor and my obsessive thinking doesnt help. I have heard of somatic illiness and I wonder if thats what OCD does sometimes. I do worry my OCD is a sign of a serious endocrine problem but I also know OCD loves to try and look for ways to protect you.

Yes, stress reactions driven by obsessive behavior or thoughts, combined with compulsions, are standard symptomatic manifestations in OCD. Have you perhaps tried cyproheptadine? It is incredibly effective for cortisol-related symptoms, as excessive muscarinic signaling can cause insensitivity to CRH, leading to high levels of CRH, which in turn results in elevated ACTH and cortisol levels. Excessive glutaminergic signaling is also noteworthy, as it is excitotoxic and exacerbates OCD symptoms. Serotonin is particularly relevant in the case of OCD.

Generally, what I can recommend for OCD includes anticholinergic and antiserotonergic medications, along with an appropriate diet low in tryptophan, oleic acid, and PUFA. Ensure adequate intake of proline and glycine, proper supplementation with vitamin D3, and consider exploring GABAergic substances, which exert a neurochemical effect opposite to that of glutamate, inhibiting nervous system activity and thereby reducing symptoms. Magnesium and zinc also have invaluable effects.

I have also heard about microdosing ketamine, which inhibits the activity of the glutaminergic system. Personally, I have used cyproheptadine, which alleviated my symptoms, although it did not alter orthorexic behaviors, which I view as positive. I do not believe it is rational to label justified, even if excessive, health-conscious behavior as pathological—unless it becomes a source of stress or results in malnutrition, which is rare.

@zaaku A very specific question, but a lack of specific information. How much do you weigh? Do you have abdominal obesity? What are the proportions of macronutrients in your diet? Do you consume an adequate amount of choline and vitamin B12? What supplements do you take, and what are your levels of triglycerides, cholesterol, TSH, cortisol, insulin, and other relevant metabolic markers? A general recommendation for treating NAFLD is weight loss.

@war4512 https://www.youtube.com/watch?v=QpZLQI_uORs&ab_channel=HardMission

A song that evokes a lot of positive emotions in me. One of the most motivating tracks.

"Because more than anything else rhythm and harmony find their way into the inmost soul and take strongest hold upon it”. - Plato

Music is an inherent component of our identity. It is a kind of mirror, transparently revealing the nature of our character. It is the most authentic marker of personality, as music leaves no room for secrets—it is an expression of ourselves. It serves both as an indicator and a driving force for our activity in the broadest sense of the term. Music motivates, discourages, and inspires all at once. The power of these specific sound waves, arranged in an artistic and rhythmic sequence, is intriguing. So intriguing, in fact, that these surprising, physical waves have unexpectedly (or expectedly) profound effects on our bodies.

Music is not merely mechanical waves perceived by our hearing organs. Different waves, rhythms, and tones impact the brain's neurochemistry in diverse ways. Music is a mechanical signal of what is about to happen in our brain.

The fundamental components of music include melody, harmony, and rhythm.

"For example, female field crickets are attracted to males that produce songs within a narrow range of pulse frequencies, and this selectivity is mediated by a network of interneurons that process instantaneous pulse frequency through a coincidence-detection mechanism (Schoneich, 2020). While pulse frequency preferences are innate in many invertebrates, experience can shape neuronal responses to pulse frequency in other species. For instance, excitatory neurons in the auditory cortex of mice are innately sensitive to the most frequent pulse frequency of pups (~5 syll/s), but their tuning can extend to a broader frequency range after cohabitation with pups producing the range of pulse frequencies (Schiavo et al., 2020)."

Neuroimaging studies have shown that the striatum and other limbic system structures are activated when people experience pleasure derived from musical signals, and these responses are relative and depend on the degree of perceived musical pleasure (Mas-Herrero et al., 2021b). Similarly, the autonomic system (increased heart rate, altered breathing) also responds relative to the subjectively perceived pleasure from music. The dopaminergic system plays a particularly important role in experiencing pleasure from music, which is linked to the limbic system. For example, it has been proven that music therapy reduces ADHD symptoms, particularly in gaming contexts (M Martin-Moratinos et al., 2023). Another randomized controlled trial demonstrated that music therapy reduces cortisol expression, lowers blood pressure and heart rate, and improves psychological scale scores symptomatically (JI Park et al., 2023).

Moreover, it has been observed that as subjective liking of music increases, functional connectivity between the auditory cortex and reward structures also increases, which has key implications for the course of musical anhedonia. A lack of connectivity between the auditory cortex and neuronal structures of the reward system is the cause of anhedonia or the lack of affective experiences in response to auditory stimuli.

"Relationships between music and cognitive or sensory functions have been largely studied in humans. Longitudinal studies have shown that many years of music education or training are associated with improved executive functions, including inhibition, planning, and verbal intelligence in school-aged children (Jaschke et al., 2018; Hennessy et al., 2019). Similarly, in older adults, musical practice benefits cognitive functions (Roman-Caballero et al., 2018), while various forms of MBIs appear to benefit cognitive functions, including short-term and working memory, digit span, orientation, fluency, abstraction, and psychomotor speed, as well as reduce pain in individuals with dementia (Hofbauer et al., 2022). A significant amount of literature also supports music as an adjunctive treatment for pain relief (Lunde et al., 2019). In contrast, relatively few studies focus on the brain mechanisms through which MBIs induce cognitive and sensory effects in humans (Chaddock-Heyman et al., 2021) or in animal models (Zhou et al., 2022)."

Thus, music is not merely a mechanical physical stimulus but a highly complex element that fundamentally influences brain neurochemistry and the central nervous system through the auditory cortex.

Reports also suggest a soothing effect of auditory stimuli on stress levels and management, likely due to adaptive and central lowering of ACTH levels at the pituitary level.

Music should not be viewed reductionistically but as broadly as possible. According to bioenergetic philosophy, music, if appropriate, can have positive metabolic inclinations; leading to increased aerobic glucose oxidation in the brain, as music can lower glucose levels, likely caused by neuronal activation at the limbic system level.

From a bioenergetic perspective, music can be a useful tool for managing our physiology by increasing dopamine, reducing stress, and boosting motivation, linked to an enhanced dopaminergic response.

As someone with ADHD, I love nu-style and old-style hardstyle, gabber, early hardcore, hard trance, hands-up, trance, and happy hardcore, which bring me the most joy and help with motivation.

Over the past few weeks, I have made a very intriguing empirical observation. For the sake of this post, I’ve called this observation the “orthorexic sequence.”

A brief explanation:

When I struggle with gut issues (pain, bloating), there is an exponential intensification of obsessive-compulsive disorder (OCD) symptoms. One manifestation of this is orthorexia and an obsessive focus on my health, leading to meticulous dietary changes that alleviate pathological symptoms. This, in turn, results in a relaxation of dietary restrictions, which leads to a worsening of health. Admittedly, for a while, I did not adhere to fundamental dietary principles. I consumed too much fat, white flour, and meat, with too few fruits, etc. I’ve noticed that this creates a causal chain.

The role of serotonin transporters (their excessive signaling) and dopamine D2 receptors is well-documented. I’ve hypothesized that an essential pathogenic factor is improper nutrition. My diet was rich in tryptophan, PUFAs, oleic acid, and other elements that directly contributed to my health decline. OCD is associated with disrupted neural transmission in the orbitofrontal cortex, anterior cingulate cortex, and basal ganglia—key components of the limbic system.

I don’t view this negatively because neurotransmitters are mechanical neurochemical signals. However, in this case, the hyperactivity of the aforementioned brain regions is tied to an excessive signaling of the need to fix the situation, which I believe stems from gut disorders. This is a pathological symptom if we consider excessive neurotransmission.

Should OCD be considered a self-destructive pathological condition or a signaling mechanism? It’s hard to say. Limbic system dysfunction undoubtedly plays a significant role, but is the aforementioned reaction not rational?

Naturally, when health is at risk, endocrine signals communicate aberrations to the brain. Per se, this is not self-destructive; on the contrary, it is a vital, selective mechanism indicating the need for changes. So where is the boundary? It’s hard to say; it depends on how negatively the individual experiences the associated symptoms.

I am unsure to what extent my reaction is a matter of OCD, but I strongly suspect that symptomatic improvement is linked to better dopaminergic and serotonergic transmission, which results from better nutrition and microbiological structure in the gut. However, when OCD symptoms subside, I tend to gravitate toward eating what I once deemed destructive.

This is why I’ve called it a sequence, due to the very pronounced deterministic chain of cause and effect. I will try to prevent this, given the logical consequences that lead to health deterioration, which I want to avoid.

The cause might be a deep dysbiosis in the large intestine or an overgrowth of microorganisms in the small intestine. The relationship between the microbiome and mental health is very well-documented in the literature.

One of the most significant dietary pathogenic factors might have been glycoproteins and microorganisms whose metabolic byproducts include endotoxins (lipopolysaccharides). A lack of fiber and fruits could also have been a contributing factor. Fiber significantly influences the production of butyrates, which regulate BBB integrity and central neurochemical regulation. SCFAs themselves are also crucial for intestinal permeability. A deficiency might exacerbate the release of endotoxins into the bloodstream.

For easier understanding, here is the sequence:

Gut disturbances → OCD → Obsessive focus on health (orthorexia) → Health improvement → Relaxation of dietary discipline → Gut disturbances.

@Mauritio said in Niclosamide reduces serotonin and glutamate:

Of course there is glycogen depletion at first when you increase your metabolism. But if that was the cause the weight loss would have shown the next day and not the day after that . Plus glycogen is quickly refilled when having meals.

Well, if you've noticed that your muscles are fuller, it’s probably because you are compensatorily consuming large amounts of glucose. T3 also has some ability to reduce glycogen, but this depends on the dose and metabolism. When I take thyroid hormones, I also notice that I’m fuller, but that’s because I consume around 600/700g of carbohydrates a day, which has a compensatory effect.

@Mauritio said in Niclosamide reduces serotonin and glutamate:

I suggest you read about the basics and benefits of uncoupling and their effects on humans. Georgi has a lot of good content on that.

I’m familiar with the process of uncoupling. It’s an extraordinary mechanism, but as I mentioned, it depends on the substance or another physiological factor that induces it. PUFA, for example, also promote uncoupling, but through PPAR-gamma, impairing biogenesis, which T3 does not do. However, if there is a noticeable increase in lactate, it is probably related to limiting OxPHOS, resulting in increased glycolysis.

@Mauritio said in Niclosamide reduces serotonin and glutamate:

The paragraph you quoted merely describes how niclosamide kills parasites.
Yes that happens through uncoupling, and yes if we uncoupled our metabolism too much we would die too (ever heard of DNP?) .

I fully agree, however, the pharmacological action of niclosamide on parasites should also have systemic effects. I didn’t say that mitochondrial uncoupling is bad – it depends on the substance that causes it. For example, T3 also uncouples mitochondria, but it has a beneficial effect. There are also uncoupling substances that cause negative symptoms.

@Samyo You probably have a high pH in your intestines, which promotes the growth of opportunistic bacteria that, by fermenting fibers, release high levels of endotoxins.

@war4512 I’ll read more about niclosamide today because it seems to me that a single study is not necessarily conclusive on this matter. Especially since it was a study conducted on carp.

@Mauritio

https://www.mdpi.com/2073-4425/14/12/2196

The weight loss is likely due to glycogen depletion and the water associated with it. What's worse, the use of niclosamide has been observed to lower CO2 levels and increase LDH levels. This makes the use of carbonic anhydrase inhibitors even more justified when taking niclosamide.

..Meanwhile, exposure to NIC resulted in a decrease in the liver glucose (Glu) level, gut cholesterol (CHO), and glycogen (Gln) and triglyceride (TG) content in all examined tissues. Conversely, it led to an increase in tissue lactic acid (LA) and acetyl-CoA levels, as well as LDH activity."

,,It is hypothesized that NIC has the ability to disrupt the process of mitochondrial oxidative phosphorylation via uncoupling. In the case of tapeworms (Cotugnia digonopora), exposure to NIC led to the accumulation of lactate, decreased production of CO2, and reduced glycogen levels, indicating a potential impairment in aerobic ATP synthesis"

@the_black_jew said in Depopulation agenda what is the long term goal?:

@war4512 just wondering if you fit a pattern

Average height, average weight, nerdy face and tall forehead, blue eyes, blond hair. Nothing special.

Despite the media hype surrounding orange juice and the absurd results of epidemiological studies suggesting a positive correlation between orange juice consumption and the occurrence of certain types of cancer (source), empirical data seems to contradict these pseudoscientific claims. Citrus juices are a biological flavonoid bomb, containing dozens of bioactive substances. At least a few of them exhibit clear anticancer properties, such as hesperidin (s), naringin (s), terpenes (s), limonoids (s), phenolic acids (s), the intact (sic!) form of vitamin C, and citrus fiber (s). While commercial orange juice may pose a problem (due to the pasteurization process, as ascorbic acid can be converted into furans, which have pro-oncogenic properties), and the lack of fiber and structural breakdown of certain phenolic compounds, as well as the origin of the orange, the statement that it contributes to cancer is at least an exaggeration. Despite pasteurization, the juice retains many of the phenolic compounds, and it exhibits many prometabolic properties, such as lowering triglyceride, VLDL, and LDL levels (source). I believe that the juice is not the ideal solution — fruit fiber has a wide range of health benefits that cannot be explained solely by the presence of other bioactive compounds. However, the juice is a very valuable source of micronutrients and carbohydrates. Personally, I consume orange juice periodically, i.e., I split it into 4 glasses or eat the equivalent of 10 oranges alternately. The exception to this is my pre-workout, which consists of baking soda (or calcium carbonate) and a liter of juice. The argument that orange juice and fruit sugar could increase IGF-1 is quite understandable and has excellent empirical inclinations, but IGF-1 should not be viewed as inherently bad. IGF-1 indeed increases after the consumption of carbohydrates or proteins in general. IGF-1 is not harmful as such when released sharply. On the other hand, chronically elevated IGF-1 is a completely different matter.

Below is a study reporting the effects of orange juice and its extract on the development of cancer cells:

Orange juice (OJ) is one of the most consumed among other CF juices worldwide, and even one of the most studied regarding its health benefits. Indeed, it is well known its antioxidant property that is due to its content of both Vitamin C and flavonoids (Constans et al., 2015). In this regard, recently we studied the antioxidant activity of an extract from orange juice (OJe) rich in flavonoids in both cell-free and cell-based experimental models. In particular, we showed its capbility of preventing oxidative stress induced by hydrogen peroxide (H2O2) in human lung epithelial A549 cells, diminishing reactive oxygen species (ROS) generation and membrane lipid peroxidation, as well as enhancing mitochondrial functionality and averting DNA-oxidative damage (Ferlazzo et al., 2015). Moreover, we demonstrated the iron-chelating activity exerted by OJe in Fe2SO4-exposed A549 cells and its induction of the antioxidant catalase, thus stopping oxidative injury induced by iron (Ferlazzo et al., 2016c). We further studied the antioxidant and anti-inflammatory activity of OJe through an animal model resembling colitis (Fusco et al., 2017) in which it counteracted cytokine generation, nuclear factor kappa B (NF-kB) activation, nitrotyrosine and poly ADP-ribose (PAR) formation, as well as enhanced myeloperoxidase (MPO) activity, increased manganese-dependent superoxide dismutase (MnSOD) expression and modulated both pro- and anti-apoptotic factors. Finally, it has been demonstrated that both OJ and OJe are capable of reducing cardiovascular risks (Buscemi et al., 2012) and exert anti-epileptic effect (Citraro et al., 2016).