Fire in a Bottle II, lipedema, adipaging, twinkie-fat

hyperlipid
fire-in-a-bottle
ros-is-the-signal
lipedema
the-croissant-diet

(Anthony) #41

This sounds good enough to try.

I’m still digesting the rest of your post and need to read it again when I have more time, but hopefully now you can reply.


(PJ) #42

Thanks. I’ve been saving notes on various stuff.

Edited to add: I have no idea why the forum here makes HUGE BOLD text here and there for no apparent reason but I have to go back to sleep since I have to get up for work before long so I can’t fix it.

So there seem to be a few things the FIOB eating plan is hoping to do:

  1. Downregulate SCD1, which UNsaturates our bodyfat and dietary fat, potentially locking people for eons into the loop of fat or super-rapid weight regain.

  2. Upregulate PPAR-alpha, I gotta look up why because I forget now (woke up middle of night, ready to go back to bed here, brain is dead)

  3. Upregulate AMPK (the below will explain why I’m sure)

So since all this is new to me I’ve been reading on them. Starting with #3, the increase AMPK thing, here’s “web-skim notes” about that, some of which I find interesting, and some of which I include because it’s baseline informative, and some of which I pursued looking for ‘stuff which increases it’.

AMPK


…There are two broad classes of polyphenolsthose that have a fused ring structure and those that dont. … It is only the polyphenol class known as flavonoids that have a fused ring structure that provides the appropriate three-dimensional properties to activate AMPK maximally. (Note: They merely mean the others aren’t water soluble. So eat them with fat, sheesh - PJ) … Even within the class of the fused-ring polyphenols (i.e., flavonoids), there are a lot of variations … colorful berries are the richest source of anthocyanins…

Hawthorn leaf flavonoids alleviate nonalcoholic fatty liver disease by enhancing the adiponectin/AMPK pathway

Hawthorn (Crataeguspinnatifida) belongs to the genus Rosaceae family of plants. The hawthorn leaf, Crataeguspinnatifida Bunge, is used for both condiment and medicinal purposes to prevent and treat metabolic dysfunctions, such as hyperlipidemia, hypertension, and cardiovascular disease in traditional Chinese medicine. However, its effects on nonalcoholic fatty liver disease (NAFLD) remain obscure. The purpose of the present study was to investigate the protective effect of hawthorn leaf flavonoids (HLF), the dominant bioactive extracts of hawthorn leaves, on high fat diet (HFD)-induced hepatic steatosis and to elucidate its underlying mechanisms.

HLF supplementation significantly lowered body weight, liver weight, liver/body weight ratio, improved serum parameters and liver dysfunction and markedly decreased hepatic lipid accumulation in HFD-fed rats. In addition, HLF intervention dramatically increased circulating adiponectin levels and up-regulated the expression of adiponectin receptors, particularly adiponectin receptor 2 (AdipoR2) in the liver. Moreover, adenosine monophosphate (AMP)-activated protein kinase (AMPK) was also activated, as well as AMPK-mediated alteration of sterol regulatory element binding protein-1c (SREBP-1c), peroxisome proliferator-activated receptor (PPAR) and their downstream targets. Taken together, our data suggest that HLF ameliorates hepatic steatosis by enhancing the adiponectin/AMPK pathway in the liver of HFD-induced NAFLD rats.

In the past decade, the discovery of numerous new AMPK substrates has led to a more complete understanding of the minimal number of steps required to reprogramme cellular metabolism from anabolism to catabolism. This energy switch controls cell growth and several other cellular processes, including lipid and glucose metabolism and autophagy. Recent studies have revealed that one ancestral function of AMPK is to promote mitochondrial health, and multiple newly discovered targets of AMPK are involved in various aspects of mitochondrial homeostasis, including mitophagy.

The SIRT1 enzyme is boosted and required by AMPK as well. Until only recently has it become apparent that they have similar effects on as cellular metabolism, inflammation, and mitochondrial function they work hand-in-hand.

Fiber is a key player in activating AMPK. A special form of soluble fiber called glucomannan that is many times more effective than any other fiber in improving insulin sensitivity and activating AMPK. … water-soluble, viscous fiber are beans, oat bran, nuts, seeds, psyllium seed husks, pears, apples, and vegetables.

AMPK (5 AMP-activated protein kinase) is an enzyme that plays a key role in energy balance. All creatures from yeast to humans have this enzyme [1].

AMPK can detect the level of energy (number of ATP molecules) in a cell and helps regulate responses when it gets too low or high.

AMPK in the hypothalamus senses our level of energy production in the body (in the form of ATP). It increases energy expenditure and can also increase appetite (when it is activated in the hypothalamus) [2].

When cellular energy is low, AMPK is activated and targets a range of processes, the net response of which is an increase in energy production and a coordinated decrease in energy (ATP) usage [3].

Hypothalamic AMPK increases appetite, increases glucose production and uptake, reduces heat production, and decreases energy output [2].

Glucose is the main source of energy for the body and is particularly essential for normal brain activity. Hypoglycemia, a condition in which the blood glucose drops below normal levels, poses a great danger to the stability and functioning of the brain and therefore activates AMPK [2].

Hypothalamic AMPK activation promotes glucose production from the liver [2] and glucose uptake into the muscles [4].

AMPK inhibits glucose storage (glycogen synthesis), resulting in more glucose being available for energy production [4].

In various cells, AMPK stimulates the breakdown of glucose for energy (in the form of ATP) [4].

AMPK inhibits the production of fatty acids, cholesterol, and triglycerides, and instead stimulates the breakdown and burning of existing fat for energy [4].

Protein production is a high-energy process that is inhibited during low energy states to conserve energy. Therefore, it is not surprising that AMPK inhibits protein production [4].

Inhibiting excessive protein production results in a much more energy-efficient and less wasteful cell.

Autophagy is the process of recycling cellular components. This process promotes molecular and cell subunit quality control by degrading damaged or misfolded proteins and even damaged mitochondria [3].

Autophagy can contribute to energy generation by providing fuel for mitochondrial metabolism, and AMPK promotes this process [4].

AMPK is capable of both acute and long-term improvement of mitochondrial activity [3].

AMPK also regulates the production and turnover of mitochondria. Loss of AMPK in mice reduces mitochondrial activity and greatly diminishes muscle performance [3].

AMPK has a crucial role in increasing antioxidant defense during oxidative stress [4].

AMPK increases the production of several antioxidant proteins, such as NRF2, superoxide dismutase and uncoupling protein 2 (UCP2) [4].

Upon hypoxia (low oxygen) at altitude or during sleep, activation of AMPK may protect against acute breathing instability. Loss of AMPK was shown to cause breathing dysfunction during hypoxia in mice [5].

Variations of gene components of AMPK has been found in high-altitude Andean populations, presumably in order to improve survival in low oxygen conditions [5, 6].

In several animal species, AMPK increases the production of sex hormones [7].

The absence of AMPK leads to reduced fertility in both sexes [7].

AMPK plays a critical role in increasing blood flow through vasodilation (widening of the blood vessels), by stimulating nitric oxide release in blood vessels [8].

AMPK outside of the brain increases fat burning, and this pathway can result in weight loss [9].

By contrast, AMPK activation in the brain increases appetite. In mice, when the activity of brain/hypothalamic AMPK was inhibited, the mice ate less and lost weight. When AMPK activity was raised the mice ate more and gained weight [10].

Ghrelin, the hunger hormone, stimulates AMPK in the hypothalamus [11].

AMPK activation gradually declines during aging. Some researchers believe that the age-related increase in chronic inflammation levels is responsible for the suppression of AMPK activity [4].

Activating AMPK may help multiple longevity pathways and promote healthy aging [3].

Many studies have shown that AMPK plays a crucial role in increasing longevity and calorie restriction-induced lifespan extension in worms, fruit flies, and rodents [4].

In worms, AMPK activation can increase lifespan by as much as 15% [12].

AMPK increases longevity by reducing protein production [3] and enhancing autophagy [3].

Longevity Pathways of AMPK

AMPK activates longevity FOXO proteins [3]
AMPK activates the master antioxidant regulator NRF2 [4]
AMPK inhibits the master regulator of lipogenesis SREBPc [3]
AMPK inhibits mTOR indirectly [3]

Longevity research is a contentious and controversial field, and the precise role of AMPK in determining lifespan is unknown. Much more research is required to determine this enzymes role in aging and longevity.

AMPK can both decrease inflammation and be decreased by inflammation.

AMPK also exerts potent anti-inflammatory effects. AMPK inhibits inflammation by indirectly inhibiting NFB, a key activator of inflammation [4].

While AMPK could have many beneficial effects in chronic inflammation, it is typically reduced in such states.

AMPK activation improves insulin sensitivity [4].

AMPK deficient mice showed impaired glucose tolerance [13].

Metformin, an activator of AMPK, is the most frequently prescribed antidiabetic drug for type-2 diabetic patients [4].

The activation of AMPK also performs a protective role in cardiovascular diseases [14].

AMPK can increase male hormones/androgens in human cells [15]. However, metformin (AMPK activator) is commonly given to women with PCOS to a good effect (PCOS is a condition with higher male hormones); much more research is required to determine AMPKs role in testosterone production.

…Overactivation or underactivation of AMPK may each contribute to neurodegenerative disease…

…AMPK activation seems to be beneficial for cancer prevention, but not for cancer treatment. More research is needed…

…AMPK can suppress PPAR alpha and PPAR gamma [17], two important proteins that regulate metabolism and gene expression…

These supplements have not been approved by the FDA for medical use and generally lack solid clinical research. … That said, numerous polyphenols have been found to activate AMPK in cell and animal studies.
These include:
Resveratrol from red grapes [19, 13]
Quercetin from many plants including fruits, vegetables, and grains [19, 13]. Note that quercetin increases AMPK in fat, liver, and muscle but inhibits hypothalamic AMPK [20].
Genistein found in a number of plants such as soybeans [19].
EGCG from green tea [19, 13]
Berberine from Berberis vulgaris, Berberis asitata and Coptis chinensis [19, 13].
Curcumin from turmeric [19, 13]
compounds isolated from Solomons seal (Polygonatum odaratum) [13].
Anthocyanins found in blueberries, bilberries, grape seed extract and pine bark extract [21].
Apigenin [22]
Zinc [23]
Nicotine (in fat cells) [24, 25] and mediates the anti-inflammatory effect of nicotine [26].
Palmitoylethanolamide (activates AMPK in fat tissue, but inhibits it in the hypothalamus) [27]
Bitter Melon (Cucurbitane) [13]
Carnitine [28]
Glucosamine [29, 30]
Extra virgin olive Oil [31]
Fish Oil EPA [32], DHA [33]
Cinnamon [34]
Astragalus [35, 36]
Reishi [37]
Ginseng/Ginsenosides. A number of ginsenosides have been reported to activate AMPK, resulting in an increased glucose uptake, decreased liver triglyceride and cholesterol levels, and the inhibition of fat production and liver glucose production [19].
Apple Cider Vinegar /Acetic acid [38], Pomegranate vinegar [39]
Rooibos [40]
Creatine [41]
CoQ10 [42]
Gynostemma [43]
Hydroxytyrosol [44]
Baicalin [45, 46]
Fucoidan [47]
Danshen/Salvia Miltiorrhiza/Tanshinone IIA [48]
Red yeast rice (monascin and ankaflavin) [49]
Arctigenin from the seeds of burdock (Arctium lappa) [13].
Panduratin from Chinese ginger (Boesenbergia pandurate) [13].

These hormone pathways stimulate and regulate AMPK activation in everyday life. Maintaining a healthy diet and exercising regularly is the best way to keep each of these hormones in balance.

Fat cells produce adiponectin [13], which serves as a starvation signal [2].

In fasting, adiponectin increases and stimulates AMPK, leading to the induction of food intake and reduction of energy expenditure. After refeeding, a decrease in adiponectin level is accompanied by blunted AMPK activity [2].

Leptin, the satiety hormone secreted by fat cells in the presence of insulin, prevents overeating by inhibiting AMPK in the hypothalamus to suppress appetite [4]. It also activates AMPK in muscle [4].

The thyroid hormone T3 increases cellular oxygen consumption and activates AMPK in the muscles [50].

Nitric oxide activates AMPK [51, 52].

Activating AMPK in the brain (hypothalamus) has the opposite effect as it does when activating it in the liver, fat, and muscles. Activating AMPK in the brain increases appetite and may increase weight gain. When its activated in non-brain tissue, it promotes fat burning.

Inhibiting AMPK in the brain likewise reduces appetite and may cause weight loss. However, no substance or strategy has sufficient evidence to support claims of activating or inhibiting hypothalamic AMPK…

Ghrelin is a hunger hormone produced in the stomach and released during fasting. Ghrelin is essential for survival during severe calorie restriction or fasting when it maintains blood glucose levels [4].

Ghrelin activates AMPK in the hypothalamus and stimulates food intake [4], however, it inhibits AMPK in the fat tissue and liver [4].
Cannabinoids stimulate AMPK activity in the hypothalamus leading to increased appetite [2]. However, it decreases AMPK in fat cells and liver, similar to Ghrelin [53].

Cortisol stimulates AMPK activity in the hypothalamus [2].

Substances that Inhibit Hypothalamic AMPK
Leptin [4]
Insulin [2]
GLP-1 [2]
Estradiol [2]
Lipoic acid [19, 13] it increases AMPK in muscles, fat and liver cells [54, 55, 56]
Quercetin [20] it increases AMPK in fat, liver, and muscle [57, 58, 59]
Nicotine [60] Smokers around the world commonly report increased body weight after smoking cessation. Nicotine-induced weight loss is associated with the inactivation of hypothalamic AMPK [60].
Ketones [61]

if you want the references the above is excerpts from https://selfhacked.com/blog/natural-ampk-activators/


But AMPK can also have its negatives:
AMPK can inhibit muscle growth and repair by suppressing mTOR
Persistent overactivation of AMPK may cause stroke and myocardial ischemia[xi][xii]
Like with anything, too much of a good thing can be still bad and not enough of the good thing is definitely bad. AMPK has to be balanced with mTOR but its still one of those things you want to keep activated consistently.

dont try this at home kids, but nicotine can have an anti-inflammatory effect specifically through AMPK activation [16].
the medicinal mushroom called reishi aids in AMPK activation

AMPK is the switch that is the link between metabolic disease, inflammation, and longevity. This switch tells our cells when to store and generate energy-containing molecules such as fat, and when to hunker down and use existing energy stores.
When switched on, AMPK triggers the use of stored energy from fats, enhances removal of fats and sugar from the blood, increases production of mitochondria, and reduces inflammation and cellular junk.
Age-induced risk factors can be tackled efficiently by boosting AMPK activity with Gynostemma pentaphyllum and trans-tiliroside from rose hips.

A PubMed search now delivers over 7,500 published articles on various aspects of AMPK. For those who are curious, AMPK is the acronym to define the enzyme adenosine monophosphate-activated protein kinase.
One such longevity factor boosted by AMPK is the SIRT1 enzyme. SIRT1 operates by silencing genes that code for unhealthy responses to stress, including the inflammatory response, excess fat storage, and new fat production.

The Dangers Of Reduced AMPK

In many ways, AMPK acts as a traffic cop, efficiently moving excess fat and sugar into our cells to be burned for energy. When we are young, AMPK keeps our metabolic functions running smoothly. Ideally, we are slim and disease-free. But as we age, AMPK signaling declines, which may quickly lead to an excess buildup of blood glucose and dangerous fat accumulation.7 This turns into a lethal combination for many aging humans.

With reduced AMPK signaling, a range of damaging conditions begins to take over a previously healthy body, often leading to an early death. These damaging conditions include:

Increased belly fat,46,47
Chronic inflammation,7,46,47
Elevated blood sugar,46-49
Insulin resistance,7,46-49
High cholesterol and triglycerides,46,47
Decreased numbers and function of mitochondria,7,46,47
Increased accumulations of abnormal or damaged proteins in our cells that lead to neurodegeneration.7,50

Conventional medicine diagnoses and treats each of the above conditions as a separate disease requiring separate medications when, in fact, they are all associated with one source: declining AMPK activity.

Another deadly impact of reduced AMPK activation is a decreased number of functional mitochondria28,51 and the accumulation of cellular garbage,7,52,53 which eventually renders cells nonfunctional.50,54,55

As scientists continue to unravel the mystery of AMPK, they are discovering that many of the known biochemical longevity factors (such as SIRT1, FoxO, and p53) are activated by normal AMPK function.7 For example, p53 is a tumor-suppressing gene that inhibits uncontrolled cell propagation. Without AMPK, these longevity genes fail to perform their duties, potentially resulting in premature death.7,32

Fortunately, research demonstrates that when AMPK signaling is boosted, these deteriorating processes are reversed,56 restoring more youthful metabolism, preventing related chronic diseases, and potentially adding years of useful, productive life.


this IS from a supplement corp it’s true but I’ve seen the other refs, seems based on public research
https://www.lifeextension.com/magazine/2014/ss/ampk

Gynostemma pentaphyllum is a plant distantly related to the cucumber. In traditional Asian medicine, it’s used to promote longevity. … It promotes AMPK activation.78,82

G. pentaphyllum not only activates AMPK, but it also shuttles excess fats into the mitochondria to be utilized for energy and safe disposal. The result is efficient energy production and a sharp reduction in unnecessary fat storage.

Results of G. pentaphyllum-induced AMPK activation include increased fat burning, as well as an increase in cellular glucose uptake. Extracts of G. pentaphyllum have other beneficial properties as well, including the ability to prolong cellular life in the face of stresses induced by oxidation, fat accumulation, and diabetes.

…leaf extracts of G. pentaphyllum activate AMPK, resulting in reduced body weight gain and fat accumulation…

In another study, this time using diabetic rats, three weeks of G. pentaphyllum supplementation resulted in improved glucose tolerance by 35% and reduced new glucose production in the liver by 29%, with a reduction in liver glycogen, the storage form of sugar.

…human study, type II diabetics who were not using diabetic medications drank a tea made with G. pentaphyllum. The results compared to controls were:
A 5-fold reduction in fasting glucose,
A 10-fold reduction in hemoglobin A1c, a measure of chronic glucose exposure,
A near 3-fold decrease in insulin resistance,
No dangerously low blood sugar episodes, which can often occur with certain oral antidiabetic drugs (especially sulfonylurea class drugs).
In another human study, those taking G. pentaphyllum significantly boosted the effects of a sulfonylurea antidiabetic drug, producing an additional fasting glucose reduction of 52.2 mg/dL compared with just 16.2 mg/dL for the drug alone.

…trans- tiliroside, extracted from plants such as rose hips

Trans- tiliroside also boosts AMPK signaling, but it triggers different downstream metabolic benefits than G. pentaphyllum.79,90,91 Combining these two bioactives (G. pentaphyllum and trans-tiliroside) provides broader AMPK activation effects than each one separately.

Scientists are now finding that trans-tiliroside increases the GLUT4 transporter in cell membranes, which helps pull excess sugar out of the blood and into cells, where it is burned for energy, thereby reducing circulating blood glucose.91

In animal studies, trans-tiliroside supplementation significantly reduces dangerous after-meal glucose spikes while also suppressing surges in insulin.92 A laboratory study of insulin-resistant human liver cells found that trans -tiliroside boosted cellular glucose consumption in a manner that compared favorably to metformin, a widely used antidiabetic drug.93

Not surprisingly, in mouse models of diabetes, daily oral administration of trans-tiliroside reduced fasting blood sugar by up to nearly 30% after 15 days of treatment, while diabetic mice treated with metformin had a near 23% reduction.80 Supplemented animals also had significant reductions in serum triglycerides and total cholesterol, while experiencing beneficial increases in HDL cholesterol levels.

And in obese-diabetic mice, supplementation with trans-tiliroside increased fat burning, lowered plasma insulin, lowered free fatty acids, and lowered triglycerides, while increasing levels of adiponectin, a protein hormone that regulates glucose and breaks down fat.90 Moreover, oral supplementation of trans-tiliroside in mice for two weeks with the human equivalent dose of 56 mg/day significantly reduced plasma glucose levels.94

Along with reducing the dangers of excess blood glucose, trans-tiliroside has been shown to battle obesity, especially by reducing cellular fat. In a laboratory experiment, trans-tiliroside also demonstrated reduced plasma cholesterol and a lower ratio of LDL to HDL (which means beneficial HDL levels increased in relation to atherogenic LDL).80

Another study showed that rose hip powder prevented obesity in lean mice on a high-fat diet and reversed weight gain and body fat mass increases in obese mice on the same diet.95 Baseline levels of glucose and insulin were lowered and glucose tolerance was improved.

An additional manifestation of AMPK activation resulted in a reduction in liver fat stores, the result of reduced fat production.95 Still more impressively, studies have now shown that trans-tiliroside can significantly inhibit the accumulation of visceral fat and gain in body weight in mice after just two weeks’ supplementation, without any change in food intake at the human equivalent dose of 56 mg/day.94


the presence of insulin was required to cause a metformin-induced increase in pAMPK in these human ovarian cells. Although previous data suggest that metformin may act via an insulin-independent pathway, our results therefore imply that insulin may be required to initiate an effect.


Activated AMPK inhibits anabolic (ATP consuming) pathways as well as stimulating catabolic (ATP generating) pathways

We have recently reported that cannabinoids can stimulate hypothalamic and heart AMPK activity and can inhibit liver and adipose tissue AMPK activity in rats … THC significantly increased AMPK activity in WT animals (hypothalamus 183±41%, heart: 218±34% of control). These responses confirm our previous data in rats. In the CB1-KO animals, hypothalamic AMPK activity was not modulated by THC injection (85±16%) suggesting that these central effects are mediated by the CB1 receptor; however, we observed a significant increase in myocardial AMPK activity (303±64%) indicating that the heart effect is not mediated by the CB1 receptor.

We suggest that AMPK activation plays an important role in cannabinoid effects both in the hypothalamus and in the myocardium.


Post exertional muscle fatigue is a key feature in Chronic Fatigue Syndrome (CFS). Abnormalities of skeletal muscle function have been identified in some but not all patients with CFS. To try to limit potential confounders that might contribute to this clinical heterogeneity, we developed a novel in vitro system that allows comparison of AMP kinase (AMPK) activation and metabolic responses to exercise in cultured skeletal muscle cells from CFS patients and control subjects.

We found four main differences in cultured skeletal muscle cells from subjects with CFS; increased myogenin expression in the basal state, impaired activation of AMPK, impaired stimulation of glucose uptake and diminished release of IL6.

/end

Will post on SCD1 and PPAR-alpha another time.


(PJ) #43

Oh it would just figure that not until I swore off eating pork would I discover this now exists :roll_eyes: :rofl:


(Edith) #44

Have you considered eating a lot more seafood since it is much higher in omega 3s than omega 6s, or does that not matter for your experiment since they are both pufas?


(A fool and his bacon are soon parted) #45

Ω-3 and ω-6 fatty acids are both essential to human life. But ω-6 fatty acids are inflammatory when over-consumed. Since they compete for the same cell receptors, we want to try to eat them in equal amounts.

As Dr. Phinney has remarked, the challenge for someone eating the standard American diet is not getting enough ω-6, but rather to avoid getting too much.


(PJ) #46

I don’t care for seafood. I take Omega 3 as a supplement though.

I eat the walmart-keto diet alas, so I mostly am going to try and eat nothing but beef and chicken breast and produce, and supplement with various stuff to help reduce the SCD1 and increase the PPAR-alpha or AMPK.

I am still pretty confused about the detail, let alone about decent let alone optimal foods on this approach.

In the end this really just becomes a CICO diet for me, with careful attention to keeping PUFA the lowest % of my calories for each meal and day as possible, and some supplements. Since it is definitely not lowcarb.


(PJ) #47

I have a question about something. So if we are attempting to increase the AMPK pathway and reduce SCD1, that is like… polarity 1 of metabolic processing. The other polarity (2) is mTOR. Obviously, the body needs both. But in FIOB stuff the idea is to work on (1). My question is this:

How … long?.. does the effort with supplements, tea, etc. last? Should I switch to the anti-oxidants-and-mTOR effort say, when I sleep? I mean it has to be present sometime after all. Or every third day? Or…?


(A fool and his bacon are soon parted) #48

Dr. Robert Lustig put the following graphic in a recent lecture, showing possible combinations of three key metabolic enzymes. The first two combinations are the healthy ones (even though combination says “cancer,” as well as “growth.” “Burning” means fat metabolism and autophagy. The other six combinations all lead to disease states. EDIT: Here is the lecture in which the graphic was shown:
https://www.youtube.com/watch?v=jpNU72dny2s


(PJ) #49

I’m operating on the base of either mTOR up with AMPK down, or AMPK up with mTOR down, mostly the latter for the FIOB stuff.

No idea WTF PI3K is. Will have to look it up.


(PJ) #50

I took the Omega 3 Quant blood test that Brad recommends.

Brad:

You can calculate your desaturase index by dividing your Oleic(18:1n9) by your Stearic(18:0)

OK. But the numbers are given in percentages, so how does that work??

Blood test 4May2021
Oleic: 20.75%
Stearic: 13.70%
20.75/13.70 = 1.514598540145985
If that is how it is done.
I would expect my # to be incredibly high.
That is nowhere near where I’d expect it to be.

Huh.

Well I got the other ratings…

Hmmmn.

I will focus on improving this.

Has ANYBODY here actually tried to improve their blood in the areas measured above (which are not what a regular doctor would measure)? And succeeded??

Edited 5/21: I want to post a recipe in here specific to this fire in a bottle stuff but I can’t post 3 posts in a row. Will someone please reply to this so I can add it. :slight_smile:


#51

let’s hear more . . .


(Anthony) #52

Yes, please share


(Robin) #53

What’s AOD? Can you give me specifics about what you use?


#54

AOD9604, It’s a peptide that is a fragment of growth hormone that was made as an anti-obesity drug. Pretty much kills fat cells. If you have everything else in order it just gives the fat loss a descent bump.


(Robin) #55

Thanks, never heard of it. I will check it out.


(Robin) #56

When I entered that into Amazon, it brought up the collagen peptides I take. I’m assuming that’s NOT the same thing??? can you tell me your specific brand, etc? maybe a link?


(Kristen Ann) #57

Try looking for it through peptide and compounding pharmacies . This one has it:
Peptide Sciences: Buy Peptides Online (USA Made)
I can’t speak to this site’s reputation. I order peptides (with an RX) through Tailor Made Compounding (they also have AOD9604).


(PJ) #58

Thank you @Jess and @Selllow by the time you posted I had gotten distracted by life. Alright where was I… well I can’t remember what recipe I even wanted to share, now… I think it was a waffle using starch and stearic. Well, if I make another I’ll post it here.

Meanwhile, my experimenting and working out macros on stuff and collecting a lot of supplements has finally finished and I start what I call the S&S or Starch&Stearic diet, tomorrow 6/22.

As it turns out, after all of my angst and research:

Most of my ordinary diet fits this one just fine already.

A few things to remove: like pork loin, bacon and mayo, and my protein ends up a bit lower just because I’m eating less food less often. Adding a daily protein drink to make sure it’s high enough to not make me weak.

A few things to add: starches, corn tortillas or masa, and potatoes. A few high SFA things: stearic powder, cocoa butter, more grassfed butter. And a variety of specific supplements.

No carb limit (except “not insane”) so higher qty of things like kefir and berries than straight keto would allow. It’s a lot like having a similar dietary plan to what I normally do, except increasing the carbs to ~moderate. Since my normal process is either ketogenic (usually) or see-food SAD (holidays), that middle-ground will be new for me.

The eating schedule will be about 20/4 but there’s so many supps all the time, it is not fasting. It is simply not being hungry after a bunch of food then a bunch of stearic in the morning.

Caveats: I am not doing what might be the ideal process here, as I am still taking all kinds of things that are classified as antioxidants, and the goal is to increase the ROS of the stearic so you don’t want to kill it with antioxidants. But there are things my body wants me to take – coQ10, Quercetin, just for example – and I need to take vitamins IMO and most are antioxidants – so I’m taking it anyway.

We will just have to see the results. This is not really about fat or weight loss now; it’s about shifting the ratio/% of fat-types in the stored tissue (as indirectly roughly measured by the blood).

I have a supplement schedule that is so ridiculous even biohacking bodybuilders would be aghast.

PRE-DAY STACK

Medication-stack, take first thing on awakening:

40mg Torsemide
Time-Release Potassium (750mg equiv)
~260mg Magnesium
400mg Co-Q10

Cannot be taken before nap/sleep or effect is suppressed.
On empty stomach is better but not required.

MORNING STACK (with protein drink and/or breakfast)

Day 0 stack (every day)
A/B stack (switched every other day)
W stack (1-2x per week)

*** 0 STACK
50mg Pregnenolone
25mg DHEA
100mg 7-Keto Metabolites
600mg Alpha-Lipoic-Acid
1g beta-Alanine
100mg Vitamin B1 (Thiamine)
Herbal Thyroid Support

*** A STACK
5KIU Vitamin D3
5KIU Vitamin A
500mcg (MK7/MK4) Vitamin K2

*** B STACK
5KIU Vitamin D3
partial or full-day dose of high-B’s liposomal vitamin+mineral complex

*** W STACK
Glandular Extracts (Thyroid Adrenal Pituitary Thymus Spleen & ginseng)
Trace Mineral complex

BRUNCH STACK SMOOTHIE
homemade milk kefir + big spoon of kefir grains
frozen berries of some kind (rasp, black, blue, strawb)
Spice blend (cinnamon, allspice, nutmeg, ginger, cloves)
humic-fulvic liquid mineral complex
IP-6 Gold (inositol hexaphosphate)
MCT Oil Powder with prebiotic Acacia
Glycine powder
BCAA powder
27g stearic acid (in 30g SApowder)

BRUNCH STACK SUPPS
Omega-3 (DHA/EPA) fats
1KIU Vitamin E
Astaxanthin
Chlorella Spirulina Blue-Green Algae
2g grassfed beef organ powder caps
Boswellia

SOLO STACK MIDDAY OR EVENING
Liposomal Vitamin C (either caps or DIY sunflower lecithin+ascorbic liquid)
Ashwaganda
Lion’s Mane
ECGC (green tea extract)

SEMI-DAILY (VARIES) LIVER STACK
Liposomal Silymarin (Milk thistle)
2g Quercetin (w/100mg Stinging Nettle)
2g MSM (for sulfur)
2g NAC (N-Acetyl-Cysteine)
partial dose of high-B’s liposomal vitamin+mineral complex
Vitamin B6 (P5P)
(other supps for liver I take with other stacks)

OCCASIONAL STACK ~3x/wk (or when fibroids ache)
Should be taken 2 hours each way from food/supps
Serrapeptase
Nattokinase
Qty is determined by asking Tek at the time

SLEEP STACK (when I get into bed)
250-500g Alpha GPC Choline
800mg Tart Cherry
magnesium (qty varies)
1g Glycine
2g Taurine
2g Lysine
2g Proline
2g Tryptophan
Turmeric-Curcumin
(Drinking water in the bedroom is ‘alkaline’ water)

DAYTIME SUPPS FOR “STARCH & STEARIC” (Fire in a Bottle)
(These are to: Reduce SCD1; Increase PPAR-Alpha; Increase UCP3)
Sterculia Oil
Jiaogulan
Various things elsewhere on these lists

FOODS FOR “STARCH & STEARIC” (Fire in a Bottle)
The last ones are less-ideal but I’m eating them anyway.
— more ideal
Chuck Beef
Potatoes
Arrowroot/Corn/Potato/Tapioca starch (used to cook w/SFA)
Grassfed Butter
Stearic Powder
Cocoa Butter
Coconut Oil
Homemade Milk Kefir
Simple produce (mushrooms, peppers, onions, tomatoes)
— less ideal
Backyard-Chicken Eggs
Berries (blue, black, rasp, strawb, usually a blend)
Chicken breast (skinless, any fat removed)
Corn Tortillas (minimal ingredients) or masa corn flour
ref: Moringa Oil (might find a place for this)

I’m eating basically 20/4 , but not religiously – if I am hungry by 8pm I will eat again. Due to my insane supplement schedule including before bed, there is no true fasting involved even if I’m not having ‘food’.

1st Food: Protein Drink with Caffeine
To make sure I am always getting enough protein
Plus it’s part of morning meditation with my guides:

1 Premiere Protein drink - 30g protein
I usually take my meds right before or after this

2nd Food: Breakfast Tacos (or alt) (usually 30-60 min after the first)
2 bkydChkn eggs scrambled with 1oz grassfed butter, salt, pepper
3 corn tortillas soft-fried in coldpressed coconut oil
4oz cheddar cheese (from a block, fresh shred)
1 Tbsp hot sauce or salsa, any kind
(option: if I have any fermented veggies I’ll try to eat a few here)
S&S Food supps right after eating: 1 dropper Sterculia Oil, 1 capsule Jiaogulan
I usually take my morning stack about 30 min after this

(alt1: no tortillas/salsa, instead 1 small potato chop-fried or baked w/butter & sourcream)
(alt2: premade bowl foods like chili verde; chili con carne; or a taco bowl)

3rd Food: Brunch Smoothie (usually 1-2 hours after breakfast)
Homemade Milk Kefir, Frozen Berries, Spices, liquid minerals,
a variety of supps (IP6, MCT, prebiotic, glycine, BCAA)
(and the S&S part 30g of the stearic powder
I take a digestive enzyme to help w/stearic
I take my smoothie stack right after this
~30 min later: S&S Food supps: 1 dropper Sterculia Oil, 1 capsule Jiaogulan

The loose approach here is this:

  • Eating during the day, with S&S supps throughout the day, with or around other supps.
  • At bedtime, BCAA and no S&S, so body can focus more on mTOR instead.

High SFA, low PUFA, supps to increase PPAR-alpha or UCP3 and reduce SCD1.

I plan to take another OmegaQuant blood test (Omega 3 Complete test) around the end of September. We will see if there are any improvements.

In the meantime, signs that it might be working are:

  1. Not being hungry all day (suggests the SFA is still circulating)
  2. Higher body temp (mine tends to be low. Except when fasting, oddly)
  3. Decent amount of energy to function esp late in the day (goes w/#1)

PJ


(Butter Withaspoon) #59

PJ that is so fascinating! Ok I am aghast at that huge detailed regime! May you truly reap many benefits from so much n=1 experimentation and commitment.

I’m intrigued because I’d have to be at the other end of the spectrum. I don’t take any supplements aside from salt on my food. I eat meat eggs dairy and vegetables and hope that it supports my body. I don’t monitor anything except occasional scale weight curiousity, and pants fit. I do put plenty of awareness into how I feel and relate it back to what I ate or how I slept. Sometimes I wish I could use a CGM for just one week to have a nice graph or two.

That’s why I love these forums, a welcome to the whole diversity of approaches :hugs: Keep us updated on your progress PJ


(PJ) #60

Thanks. My ratio is a lot lower than I would expect but I bet it was nearly a full point higher before I began low carb so many years ago. It’s by mere chance that I have eaten almost no PUFA except once in awhile, pork loin, bacon or mayo – but none of them very often – everything else has been either chicken breast trimmed of fat, or 80/20 chuck, or cheese, or grassfed butter. So I was on a low-pufa diet for many years I just didn’t know it. My number is 1.5+ which is still too high mind you – about 0.8-1.2 is the range it should be in – but I bet that is so much better than it was. Lots of other people testing, including those much leaner than me, are getting results like 1.8-2.2.

I have just found and fallen in love with water kefir. I’m already a milk kefir fan. I didn’t do water because I was lowcarb. But now that I am more moderate carb, I figured I could try it. It’s quite lovely, over-fermented like I do everything, with some lime in it for example. Hoping it helps with the gut biome and leaky gut issues, nearly everything I’m doing aside from the “fat ratio” efforts, are about fixing leaky gut and improving lower gut biome.

Most of these are not easy to measure. It’s more a long-term gradual improvement hope than a “stand on the scale and evaluate how it’s going.”

PJ