ketogenic diet

[Anonymous No.14610601]

I'm here because /fit/ is retarded and can't help me
AFAIK ketosis happens when there is a low amount of carbohydrates available for energy
So the body starts making ketone bodies out of fat for energy
But then there's this bullshit about "getting kicked out of keto" for eating carbs and artificial sweeteners
>sweetener x with 0 calories kicks you out of keto but sweetener y with 0 calories doesn't
>you need to eat 15-20g of carbs a day otherwise you're not in ketosis
How could an artificial sweetener with zero calories, meaning the body doesn't use it for energy, cause me to stop using fat as energy (kicked out of ketosis).
Apparently it has something to do with insulin response, but I have no carbs I have to use something for energy and artificial sweeteners provide no energy.
Also, if I consumed 50 grams of carbs or 200 calories of carbs a day, supposedly I wouldn't be in "ketosis", but 200 calories is roughly 10% of a sedentary male's daily energy expenditure. The other ~90% would have to be a combination of fat burning and amino acid breakdown.
Also
>eat 50g of carbs or 200 calories
>run 2 miles and burn ~200 calories
I just used all of the glucose in my bloodstream that I just ate, but apparently I'm not gonna be in ketosis the entire day because I had 50g of carbs instead of 15-20.

[Anonymous No.14610617]

dont listen to ketofags...they are all fat...ask them to post body with timestamp...they wont do it

[Anonymous No.14610624]

>>14610601
Ok, try to avoid most artificial sweeteners mostly because they're terrible for you and they also give you terrible cravings for more of them. Do 25 carbs with nearly all of them being from vegetables a day. Look at net carbs: total-fiber, on all of your food labels and nutrition content. Weigh your food in grams with an electric scale. Most of the weight you lose in the first few weeks is just going to be water weight. You need to counter that a little with getting enough potassium and sodium to hold onto electrolytes. Make sure you take a calcium supplement. High protein can fuck up your ability to absorb calcium.

[Anonymous No.14610627]

>>14610624
Ah. Slowly add things back like berries, then melons that aren't watermelon. Add things back by the week after 2 weeks, slowly adding 5g more to get up eventually to about 40g. If you notice a gain, go back by 5g.

[Pax No.14610636]

>>14610601
Congratulations retard, you got memed on. Eat only meat for just a couple of years and your brain will have aged massively and you'll develop early-on-set Alzheimer's due to all the iron accumulation.
Saturated fats and animal protein promote dysfunction in the gastrointestinal barrier leading to a leaky gut that allows bacterial endotoxins into our bloodstream. These molecules promote inflammation and endolysosomal deacidification throughout the body through actions on TLR4 which increases the activation of microglial cells and macrophages. Endotoxins promote the breakdown of the blood-brain barrier allowing kynurenic acid and quinolinic acid into the brain. Endotoxins promote inflammation and insulin resistance within the brain. Increased inflammation within the brain changes the neurotrophic activities of growth factors like bdnf to favor the production of microglial cells over that of neurons.
Endotoxins by reducing insulin sensitivity within the brain and promoting inflammation increase the tone of cortisol expression which increases endocannabinoid signaling to mitigate the effects of chronic mild stress.
Chronic mild stress promotes disinhibition of GABA/somatostatin release within the brain and the internalization of GABA receptors leading eventually to disinhibition of glutamatergic activity which chronically activates neurons and under the circumstances of increased neuroinflammation insulin resistance within the brain leads to reduced neurotrophic insulin signaling, and feeds forward to promote more neuroinflammation.
Tumor necrosis factor which is increased by endotoxins that activate TLR4 and TLR2 within the body directly contributes to neuronal cell death by inducing microglial inflammation through activation of kv1.3channels. This also promotes neuronal insulin resistance and contributes to hypothalamic neuroinflammation which is the root cause of all metabolic and neurodegenerative disorders.

[Pax No.14610637]

>>14610601
>>14610636
There are metabolic ward experiments and feeding trials showing the direct consequences of consumption of high fat, high protein meal on markers of endothelial function: increases in markers of peripheral inflammation, reduction in serotonin metabolism in the brain, and these can be extrapolated to disease pathology because we can observe the direct consequences of lipotoxicity and endotoxicity within the brain and reduction in cognitive function and metabolic homeostasis through an understanding of the hypothalamic model of metabolic disorder
pubmed.ncbi.nlm.nih.gov/28677618
pubmed.ncbi.nlm.nih.gov/9036757
ncbi.nlm.nih.gov/pmc/articles/PMC2858203
pubmed.ncbi.nlm.nih.gov/28045396
pubmed.ncbi.nlm.nih.gov/19116375
ncbi.nlm.nih.gov/pmc/articles/PMC2853195
ncbi.nlm.nih.gov/pmc/articles/PMC4424797
pubmed.ncbi.nlm.nih.gov/28323986
ncbi.nlm.nih.gov/pmc/articles/PMC6506390
ncbi.nlm.nih.gov/pmc/articles/PMC6814438
sciencedirect.com/science/article/pii/S2211124716307331
ncbi.nlm.nih.gov/pmc/articles/PMC2728689
ncbi.nlm.nih.gov/pmc/articles/PMC5813603

You only ever get one brain, stop being such a careless retard with it.

[Anonymous No.14610695]

>>14610636
>a bunch of jargon
Okay, so why do people report great results when it comes to weight loss, cognitive function, and even improvements in various diseases on keto/carnivore diets? Explain Jordan and Mikhalia Peterson.
Also, all of this jargon indicating that eating animal protein and saturated fats is destroying my body and brain is not at all whatsoever corroborated by anything I can or have observed in my actual life. If all of this was true I would expect to observe these facts producing real, tangible deleterious effects in people's lives on a scale that would be readily recognizable, and it's not, therefore, I don't give a fuck. I was vegetarian for 4 years, I had no muscle whatsoever, and I was diagnosed with depression.
>>14610637
Oh, so before agriculture when humans spent all their time hunting animals on the savannah, our bodies were evolving and adapting in such a way that the hunter gatherer diet was actually incredibly damaging to the body. That makes a lot of sense.
>>14610624
Thanks. I am still concerned about what it means to be "kicked out of ketosis" and whatnot. And yeah I've been slamming artificial sweeteners recently it's not good.

[Pax No.14610708]

>>14610695
>hurr durr I disagree
>please read my schizo rambling with no sources
no thanks, retard. I posted sources so you will too.
People in the middle ages died in their 50s if they were lucky and Noblemen suffered from a variety of pathological conditions such as gout, and other diseases of affluence that everyone in the western world is easily susceptible to due to gluttony. Peasants in the middle ages likely ate healthier than kings and were more physically active because they subsisted on beans and whole grains. Quite literally all processed food we know of today was first introduced as foods of affluence. White flour and sugar were foods of kings. I consider meat a processed food because animals consume all of this plant matter and you lose all of the antioxidants, fiber, phytonutrients, carbohydrates, etc.
Nutritional anthropologists used to even consider the diets of rural Africans (which included a much larger proportion of plant foods) inadequate in protein compared to English diets.
You are misconstruing appeal to authority and epistemological arguments as an evidence-based review of nutrition. There have been several hundred years of nutritional research since the time of hunter and gatherers or kings and paleolithic man that can give us a better understanding of the molecular mechanisms of nutrition up to the cellular level.
Directly increasing neuronal insulin sensitivity increases metabolic homeostasis and BCAA catabolism. The failure of BCAA catabolism aggravates organ fibrosis, cancer growth, etc
Consuming a plant-based diet promotes lower body iron accumulation than heme iron while having similar hematocrit levels.
Consumption of phytonutrient-rich plant foods such as cruciferous vegetables and high amounts of fiber from foods like beans increase butyrate production in the gastrointestinal tract which preserves the gastrointestinal barrier.

[Pax No.14610710]

>>14610695
>>14610708
Consuming meals rich in carbohydrates increases tryptophan uptake into the brain which is metabolized into serotonin and then that serotonin activates cells within the cerebellum that increase insulin transport into the brain. This supports why a diet low in BCAAs increase metabolic health is because BCAAs compete with tryptophan for metabolism and this increases cortisol release and cms.
The loss of insulin sensitivity also reduces BCAA catabolism in the body which promotes tumor growth and acceleration of aging

As I said, it's your choice. It's all mechanistic and has been proven again and again. Just read the studies, or don't, if you want to get Alzheimer's.

[Anonymous No.14610722]

>>14610636
>Not Op.
someone said mercury increases iq. I couldn't find a source for that. What are your thoughts?

[Anonymous No.14610733]

>>14610695
Yeah. Don't listen to this faggot that shills the iron chelator. He'll be dead in a max of 5 years from conditions of severe anemia.

[Pax No.14610744]

>>14610733
It's demonstrated that opioids induce endolysosomal deacidification in our neurons which promotes iron accumulation in the cytosol. This provokes a functional iron deficiency in the mitochondria and upregulation of ferritin heavy chain within the cytosol and this locks of iron that can't serve proteostatic functions. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6675873/ free iron that's accumulated through a variety of neuroinflammatory insults such as chronic cortisol induced CMS pathology provoking glutamatergic disinhibition on pyramidal cells provokes the synthesis of allopregnanolone
https://pubmed.ncbi.nlm.nih.gov/23227932/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578010/ and it can be demonstrated that chronic intermittent allopregnanolone provokes the functional defecits observed in CMS by inducing a tolerance to allopregnanolone through provoking microglial synaptic pruning through TPSO activation and this and other
mediating factors provoke the endocytosis of gaba a receptors, provokes the reduction in somatostatin release from sst interneuron reducing their functions.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031054/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3245370/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3766825/ It could be demonstrated that some drugs in the SSRI class provoke allopregnanolone synthesis and SSRI induced sexual dysfunction may be a functional consequence of exacerbation of CMS pathology through allopregnanolone tolerance and endocytosis of GABA a receptors provoking glutamatergic disinhibition. Chronic stimulation of gaba a receptors by allopregnanolone provokes the synthesis and release of Neuropeptide FF which acts as a functional endogenous antagonist of mu opioid receptors blocking the activation of mu opioid receptors by endorphins which also contributes to this pathology. Administration of a neuropeptide ff antagonist
reverses opioid tolerance. https://pubmed.ncbi.nlm.nih.gov/16407169/

[Pax No.14610748]

>>14610733
>>14610744
From the paper: Tolerance to allopregnanolone with focus on the GABA-Areceptor
>Changes during acute and chronic stress Allopregnanolone and THDOC are released during stress as stress activates the hypothalamuspituitary-adrenal axis that releases corticosteroids, including THDOC and allopregnanolone (Purdy et al., 1991; Serra et al., 2000; Reddy, 2003). Metabolites of glucocorticoids have also been shown to enhance the GABA-A receptor effect of allopregnanolone (Stromberg et al., 2005). The
>neurosteroid allopregnanolone has previously been shown to interfere with noradrenergic and corticosteroid-mediated regulation of corticotrophin-releasing hormone release and gene transcription (Patchev et al., 1996). Those observations indicate that allopregnanolone might affect the neuroendocrine response to acute stress by influencing the hypothalamus-pituitary-adrenal axis (Patchev et al., 1996; 1997;). A repetitive stress condition in animals has been shown to result in alterations in function and sensitivity of the GABA-A receptor (Deutsch et al., 1994; Serra et al., 2000 Dong et al, 2001; Guidotti et al., 2001; Biggio et al., 2007), pointing to the possibility that chronic stress condition is related to the development of tolerance against GABA-A receptor active compounds from the adrenal glands
Rreatment with allopregnanolone is a measure to determine allopregnanolone tolerance. I do not interpret it to be a treatment of cms, Its tantamount to the administration of benzodiazepines for the mitigation of general anxiety disorder.Its demonstrated in the gaba deafferentation hypothesis that increased inflammation in the periphery increases gabaergic tone and this provokes allopregnanolone synthesis in the liver hyperammonemia and hyperbilrubinenemia provoking the activity of Heme oxygenase which provokes

[Pax No.14610749]

>>14610744
>>14610748
the breakdown of heme into carbon monoxide, and iron and this provokes the accumulation of iron within microglial cells.
https://pubmed.ncbi.nlm.nih.gov/33212416/
Heme oxygenase-1 (HO-1) is an inducible enzyme known for its antiinflammatory, antioxidant and
europrotective effects. However, increased expression of HO-1 during aging and age-related neurodegenerative diseases have been associated to neurotoxic ferric iron deposits.
I believe the best course of action for mitigating the pathology of hepatic and diabetic enchephalopathy and gabaergic deafferentation is the administration of agents that mitigate the endocytosis of gaba receptors such as BDZ antagonists, such as the endogenous gaba a antagonist pregnenolone. It's demonstrated that
reduced insulin transport and dysfunction in insulin sensitivity in our hypothalamus leads to defects in neuronal steroidogenesis of pregnenolone and that allows for the accumulation of cholesterol into lipid rafts and a further exacerbation of neuroinflammation as pregnenolone serves important functions in mitigation of neuroinflammation and introducing pregnenolone to the brain mitigates and reverses the synaptic defecits and astrocytic swelling from hyperammonemia https://pubmed.ncbi.nlm.nih.gov/35108514/
Obesity and type 2 diabetes are associated with cognitive dysfunction. Because the hypothalamus is implicated in energy balance control and memory disorders, we hypothesized that specific neurons in this brain region are at the interface of metabolism and cognition.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4835883/

[Pax No.14610750]

>>14610733
>>14610744
>>14610748
>>14610749
This study demonstrates that neuroinflammation contributes to an increase in gabaergic tone as a defect in neuronal insulin sensitivity, glutamatergic homeostasis from reduced activity of glutamate transporter leads to glutamatergic disinhibition and chronic hyperammonemia induced activation of pyramidal cells provoking release of allopregnanolone. Its this disinhibition of gabaergic signaling within the periphery and within the brain that contributes to somatostatin dysfunction and transcriptional drift leading to a disinhibition in endozapine synthesis as gaba interferes with the functional activity of somatostatin interneurons by promoting the hyperpolarization of gabaergic interneurons leading to an exacerbation in glutamatergic disinhibition
pubmed.ncbi.nlm.nih.gov/16033417/
pubmed.ncbi.nlm.nih.gov/16033415/
www.ncbi.nlm.nih.gov/pmc/articles/PMC3180997/
This is known as the gabaergic deafferentation hypothesis of brain aging and it interfaces with the hypothalamic inflammation model of metabolic disorder and cognitive decline due to functional defects in insulin transport to the brain, pregnenolone steroidogenesis, processing of cholesterol and the accumulation of sphingolipids, defects in cerebral glucocereboxidase activity, ferritin turnover within the brain and this leads to functional iron deficiency leading to defects in proteostasis.
pubmed.ncbi.nlm.nih.gov/8717636/
pubmed.ncbi.nlm.nih.gov/9527011/
pubmed.ncbi.nlm.nih.gov/8159265/
www.ncbi.nlm.nih.gov/pmc/articles/PMC4465775/
onlinelibrary.wiley.com/doi/full/10.1002/jha2.321 Its demonstrated that insulin provokes the exocytosis of gaba, nmda, and ampa receptors to their cell surface and this is due to an increase in neuronal atp genesis from glucose stimulated energy metabolism and this accelerates the transport of mitochondria to synaptic vesicles.

[Pax No.14610755]

>>14610733
>>14610744
>>14610748
>>14610749
>>14610750
>>14610698
>>14610689
>>14610692
>>14610696
This is supported by the first study I shared supporting the evidence that endolysosomal deacidification from opioid receptor stimulation provokes iron accumulation in the cytosol and is responsible for the opioid induced synaptic defects and neurotransmission and quite possibly reduction in neurogenesis as well. Deferoxamine completel reverses these defects observed with morphine administration It's demonstrated that ICV deferoxamine is protective against subarachnoid hemorrhage as well as intranasal deferoxamine and heme oxygenase may be partially why deferoxamine is neuroprotective. https://pubmed.ncbi.nlm.nih.gov/27618864/ It's shown that heme oxygenase activators potentiate the analgesia from opioids and provoke the exocytosis of opioid receptors to the cell surface. https://pubmed.ncbi.nlm.nih.gov/25204546/ https://pubmed.ncbi.nlm.nih.gov/23358127/ https://pubmed.ncbi.nlm.nih.gov/26730587/
Intranasal deferoxamine has 200 fold higher brain exposure that peripheral administration and has significantly lower systemic exposure while eliminating the neccesity of lengthy multiple hour long intravenous injections. https://pubmed.ncbi.nlm.nih.gov/19509317/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7911954/
https://sma.org/abstracts/intranasal-deferoxamine/
https://smaorg-bucket.s3.amazonaws.com/video/PIT/2021_PIT/Abstracts/Session6A_B/Kosyakovsky.mp4

There is not a shred of evidence to what you're saying. Intranasal deferoxamine is not systemic and has never been shown to decrease blood iron levels.

[Anonymous No.14610764]

>>14610601
>I just used all of the glucose in my bloodstream that I just ate

glucose stored in the muscles can last many days. your sweetener has sugar or promotes proliferation of "bad" gut bacteria. so long as you fast appropriately, getting kicked out of ketosis isnt the end of the world. i use the keto fast mimicking diet to fast track my progress. takes as few as two days to get back into ketosis.
https://thenutritionalhealingcenter.com/fasting-mimicking-diet/

[Anonymous No.14610780]

>>14610755
What is your day job?
NTA

[Anonymous No.14610881]

keto works if you're fat and sedentary for a couple weeks, but youre just losing water weight and keeping your muscle glycogen low all the time...unless youre trying to win a weight loss contest there is no point

[Anonymous No.14610957]

There are no inherent benefits to ketosis itself, unless you're diabetic, and even then it's debatable.
The benefits of keto diet can mostly be attributed to the fact that you cut out a lot of processed shit and eat more veggies.

Artificial sweeteners will not take you out of ketosis, if they are 0kcal. They do not raise blood sugar. They are fine unless you go overboard, which can lead to GI issues such as bloating. Some sweeteners degrade in high heat, so some are not recommended for cooking/baking. They MAY increase your appetite, according to SOME studies.

>if I consumed 50 grams of carbs or 200 calories of carbs a day, supposedly I wouldn't be in "ketosis"
Ketosis takes a while to reach, your body has to burn through glucose stores first. When you reach ketosis, and then eat 50g of carbs, you will burn them pretty quickly and get back to ketosis in a few hours, probably.

What is your goal with keto diet, anyway?

[Anonymous No.14610989]

>>14610695
>Okay, so why do people report great results

not to mention that humans evolved on such a diet

[Anonymous No.14611001]

>>14610989
>tfw haven't found any mammoth to hunt for a few days
>tfw cannot eat forest berries because they have carbs and I'm on keto

[Anonymous No.14611009]

>>14610989
Nta, but I don't see carbohydrates as a distinct enemy so much as that grains are usually processed into oblivion into foods that our bodies don't deal well with. Doing lower carbohydrate diets encourages us to drop those addictions and overly processed foods. There's alternatives for foods like pastas that are made exclusively with lentils or chickpeas, and have incredibly high fiber and protein content. They taste pretty vegetal. The lentil one was a powerful beast that couldn't be tamed by strong marinara sauce and sort of tasted like old pot, but it's a future option that's less fucked than gobbling down enriched wheat products.

[Anonymous No.14611021]

>>14611009
What are
>rice
>oats
>whole grain flour
>quinoa
>lentils
>chickpeas
>potatoes

You don't have to eat either nothing or highly processed products made from refined bleached grains. Just cook your own food ffs.

[Anonymous No.14611026]

>>14611021
Whole grain flour tastes like dog ass unless it's in a good 7 or 12 grain. You don't have to remove all of those things permanently, but low carb diets are a great way to reset things and slowly reintroduce them to find foods that are problems. Plus it helps kill cravings for processed garbage because of going cold turkey.

[Anonymous No.14611180]

>>14611009
all agricultural societies fall to the diseases of civilization

https://www.youtube.com/watch?v=7kGnfXXIKZM

[Anonymous No.14611182]

>>14611001
>>tfw haven't found any mammoth to hunt for a few days

literally nothing wrong with that. and meat stores well.

>tfw cannot eat forest berries because they have carbs and I'm on keto

berries are fine grug. eat any good books lately?

[Anonymous No.14611348]

>>14610957
>Ketosis takes a while to reach, your body has to burn through glucose stores first. When you reach ketosis, and then eat 50g of carbs, you will burn them pretty quickly and get back to ketosis in a few hours, probably.
See that's what I was thinking but I kept hearing everywhere "DONT EAT 30G OR UR KICKED OUT OF KETO AND KETO TAKES X DAYS TO GET BACK INTO"
>There are no inherent benefits to ketosis itself
People do report cognitive benefits ostensibly from the brain running on ketones
>What is your goal with keto diet, anyway?
I became highly addicted to carbs the last couple months and would eat cereal and oatmeal continually all day long, so I'm trying to repair that.
Also I want to lose fat quickly because my previous diet was not conducive to cutting.

[Anonymous No.14611412]

>>14611348
>People do report cognitive benefits
That's a weak ass evidence. There is no good data for this and the several studies I checked were pretty poorly designed with somewhat random results. It probably does fuck all.
>became highly addicted to carbs
Fair enough. Low carb/keto is pretty good for lowering calories. I'd just watch my saturated fat intake desu.

[Anonymous No.14611612]

What are you eating that has 200 calories in 50 grams?

[Anonymous No.14611617]

>>14610881
Where is that water coming from? Cells are mostly made up from water, so if you're losing fat cells it would stand to reason that you're also losing water

[Anonymous No.14611621]

>>14610957
The benefit with keto is that it generally keeps you feeling pretty full. Fat and protein keeps your hunger at bay pretty well, so it's easier to eat fewer calories because you're not getting as hungry

[Anonymous No.14611677]

>>14610881
The point is to minimize circulating insulin and glucose. Chronic high levels of both of these are bad for you.

[Anonymous No.14611681]

>>14611677
That's called diabetes. You're not going to have chronic high levels of insulin and glucose from eating carbs if you don't have diabetes.

[Anonymous No.14611712]

>>14610957
>There are no inherent benefits to ketosis itself, unless you're diabetic, and even then it's debatable.
The benefit would be reducing average circulating insulin and glucose. Also, you reduce blood sugar spikes, which in themselves oxidize lipoprotein(a) which is a recipe for athrogenicity. Keto also has a tendency to reduce serum triglycerides and raise (HDL) cholesterol.
>The benefits of keto diet can mostly be attributed to the fact that you cut out a lot of processed shit and eat more veggies.
If you are talking about weight loss, this is not true. The weight loss is caused by reducing circulating insulin. Insulin inhibits lipolysis (burning and using fat for energy) and it promotes fat storage. So you won't start burning fat as long as you have high circulating insulin. You get high circulating insulin from eating carbs. Eat less carbs, circulating insulin drops, the body gets signalled to use strored fats.

Insulin Inhibits Lipolysis in Adipocytes via the Evolutionarily Conserved mTORC1-Egr1-ATGL-Mediated Pathway
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3753874/

[CarbEnjoyer !kzyHi3j84o No.14611729]

>>14610617
This tbqh, they can't prove what they preach.
The body is not retarded enough to see a massive calorie surplus, and then not only store literally none of it, but then burn more for no reason just because you didn't have a bun on your triple bacon cheeseburger.
>>14610601
Nothing wrong with the diet itself. It's not like the food you'll have to eat isn't nutritous. Especially if you have stuff like organ meats and eggs you'll get your micronutrient needs.

[Anonymous No.14611737]

>>14611681
>You're not going to have chronic high levels of insulin and glucose from eating carbs if you don't have diabetes.
Not true at all. At least with regard to insulin. Your body can keep the fasting blood glucose and A1C under the pre-diabetes/diabetes level while at the same time becoming insulin resistant and releasing even larger amounts of insulin. It takes more and more insulin to hold the number down. The best diagnostic for insulin resistance and as a marker for predicting type-2 DM is the kraft test by the way.
Postprandial insulin assay as the earliest biomarker for diagnosing pre-diabetes, type 2 diabetes and increased cardiovascular risk
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5708305/

>Meridian Valley Lab’s Kraft Prediabetes Profile is a timed test that measures the patient’s insulin response to a measured glucose challenge and return to baseline over a 4-hour period. This test looks at patterns of insulin response rather than a strict cut-off point for glucose. These patterns delineate the severity of insulin resistance, as a patient progresses from normal insulin sensitivity to postprandial hyperinsulinemia to the insulinopenic state found in beta-cell exhaustion. This spectrum of insulin response allows the clinician to identify insulin resistance early in its development. The resulting evaluation of insulin resistance severity can be used to monitor efficacy of treatment.
https://www.meridianvalleylab.com/services/kraft-prediabetes-profile/

[Anonymous No.14611778]

>>14611681
If you look at this graph, you will see the lingering insulin spike postprandial. Those will eventually be accompanied by the higher blood sugars. All the attention in terms of harm is usually given to hyperglycemia, but hyperinsulinemia is in itself a terrible thing to have. It is particularly bad for the cardiovascular system.


Insulin as the Real Culprit
https://blog.designsforhealth.com/node/633

[Anonymous No.14612527]

I've been on keto for about 2 months before I decided to stop because I wasn't getting what I want from it. I don't care about weight loss as much as I care about the psychological and physical benefits of this diet.

When I started I felt like a frail water sandwich for 5 days and on the 6th day I felt mentally and physically energetic. I instantly got out of bed without lazing about for 1-2 hours. I was focused, attentive, patient and barely felt any hunger even though I hadn't eaten anything for 14 hours. What was the most surprising is that I had virtually no anxiety or depression-like feelings. I also felt less excitable and less prone to emotional highs. I'm generally a shy person so I don't talk at all to strangers, yet on that day I felt less inhibited and talked to a couple strangers without any nervousness at all. I felt that way throughout the whole day. A couple days later I drank 2 cans of beer and ate a pack of peanuts, which kicked me out of ketosis. Ever since I'd get the increased energy on some days and not others. Over time it stopped happening completely and I felt no different than when I eat normally, so I stopped to experiment. I ate carbs with no limit for about a month and decided to try keto again. This time I didn't feel tired at all. I only felt bad if I didn't supplement electrolytes. I didn't feel the benefits this time either so I stopped to try and figure out what is happening and why it's not working.

What I ate throughout those two months: Salmon, chicken, tomatoes, celery and fat. I was eating under 10 g of carbs a day.

tl;dr - Did keto. Felt good briefly but then I messed it up. Got into it again but it only worked sporadically and over time the benefits disappeared completely. Tried it again but it's not working. Why is it not working?

>inb4 you felt better because you changed something in your life/stopped eating garbage
I don't think it's because of that. I'm not sure about this, but I think BHB acts like a mood stabilizer.

[Anonymous No.14613154]

>>14611001
>>tfw haven't found any mammoth to hunt for a few days
kek you are obviously a dumb city kid with no knowledge about jerking and smoking meat, that lasts for weeks to months.

[Anonymous No.14613170]

>>14610601
>How could an artificial sweetener with zero calories, meaning the body doesn't use it for energy, cause me to stop using fat as energy (kicked out of ketosis).
Sucralose increases insulin.
OP you’re fat aren’t you? Why don’t you just stop coping? Stop being addicted. You’ll go on keto then eat oatmeal.

[Anonymous No.14613536]

>>14612527
Does anyone have any idea why it doesn't work? I really want to feel like that again.

[Anonymous No.14613547]

>>14610601
You can't metabolize glucose without lead. The speed of fat burning is limited by available cadmium (cadmium kicks off fat burning and spares glucose) and mercury may allow gluconeogenesis from fatty acids.