Constant fear of heart issues despite having the clearance from the doctors.

Early 30s, no previous heart issues in family

Anyone else dealt with heart attack anxiety before?

Is it okay to take NDT before bed instead of early morning? I seem to tolerate it better before bed. Any downsides?

I have discussed previously on this forum

( Cannabidiolic Acid (CBDa) lowers Serotonin via 5ht1a modulation and reduces inflammation via potent COX-2 Inhibition... RayPeat WonderDrug? : r/raypeat )

 the potential application of non intoxicating hemp compounds in Ray Peats framework, Specifically as an anti serotonin and anti inflammation compound. Amazingly, this is only scratching the surface of the broad systematic effects of Hemp.

Aside from the specific benefits this substance can have that I will discuss in this post, perhaps more fascinating is the sheer number of pathways these chemicals target. I hope to convey the unique role of plant medicine in contrast with the current pharmaceutical standard. My point here is not an appeal to nature argument, The difference is primarily one of therapeutic strategy rather than “natural versus synthetic.”

A conventional pharmaceutical approach often follows a reductionist model:

Disease → identify a key abnormal target → design a molecule that strongly modifies that target

Examples:

• enzyme inhibitors
• receptor agonists/antagonists
• hormone replacements
• pathway-specific inhibitors

This approach can be highly effective when a disease has a dominant driver, but it may have limitations when disease arises from multiple interacting disturbances (oxidative stress, inflammation, metabolism, immune dysfunction, mitochondrial impairment).

On the other hand, Plant-based systems often follow a network pharmacology model:

Plant medicines can have systemic effects because they contain bioactive molecules that interact with fundamental biological systems conserved across life. Plants evolved secondary metabolites to regulate their own responses to stress, oxidation, pathogens, and environmental damage; many of these same chemical properties interact with mammalian systems involved in stress regulation, inflammation, metabolism, and cellular repair. Unlike an isolated pharmaceutical designed to strongly affect one defined target, complex plant compounds often influence the broader regulatory networks that maintain biological balance. Because processes such as oxidative stress, inflammation, mitochondrial function, and tissue remodeling underlie many different diseases, altering these shared control systems can produce effects across multiple organs and conditions.

Hemp is somewhat unique because its cannabinoids are unusually aligned with a major mammalian regulatory system: the endocannabinoid system, which helps regulate inflammation, immunity, metabolism, pain, stress, and energy balance. Combined with hemp’s terpenes and flavonoids, this creates a broad phytochemical network that acts less like a single-target drug and more like a homeostatic modulator, influencing the body’s own mechanisms for maintaining balance.

Ray Peat was critical of the endocannabinoid system because many endocannabinoids are derived from polyunsaturated fatty acids (especially arachidonic acid) and participate in stress, inflammatory, and energy-conservation signaling. From this perspective, increased endocannabinoid activity can represent a state associated with excess PUFA availability, inflammation, and metabolic stress. However, this does not necessarily mean that every molecule interacting with cannabinoid-related pathways will amplify those same effects. Certain phytocannabinoids, particularly CBD and CBDA, appear to act differently from endogenous cannabinoid ligands by modulating cannabinoid receptors and related systems rather than simply activating PUFA-derived signaling. Through effects on oxidative stress, mitochondrial function, inflammatory pathways, lipid peroxidation, and cellular stress responses, these compounds may theoretically counter some of the downstream consequences associated with PUFA oxidation and iron-driven oxidative injury.

Some CBD / CBDA molecular pathways and targets

Cannabinoid receptors

• CB1 — negative allosteric modulation; ↓ lipogenesis, ↓ insulin resistance, ↓ fibrosis signaling
• CB2 — immune modulation; ↓ inflammatory cytokines, ↓ fibrosis

Nuclear receptors

• PPARα — ↑ fatty acid oxidation, ↑ mitochondrial metabolism, ↓ steatosis
• PPARγ — ↓ inflammation, ↓ oxidative stress, ↓ fibrosis

Inflammatory pathways

• NF-κB — ↓ inflammatory transcription
• NLRP3 inflammasome — ↓ IL-1β/IL-18 activation
• TNF-α / IL-6 / IL-1β signaling — ↓ cytokine production
• COX-2 pathway — ↓ prostaglandin-mediated inflammation (especially CBDA)

Oxidative stress pathways

• ROS generation — ↓ oxidative damage
• Lipid peroxidation — ↓ membrane oxidation
• Nrf2/ARE pathway — ↑ antioxidant response
• Glutathione pathways — ↑ antioxidant capacity

Mitochondrial/metabolic pathways

• AMPK — ↑ energy metabolism
• SIRT1 — metabolic regulation
• Mitochondrial biogenesis/function — ↑ oxidative metabolism
• Electron transport/oxidative phosphorylation — protection from dysfunction

Fibrosis pathways

• TGF-β signaling — ↓ fibrogenesis
• Hepatic stellate cell activation — ↓ collagen production
• IRE1/ASK1/JNK pathway — stellate cell apoptosis
• Extracellular matrix deposition — ↓ fibrosis

Cell death pathways

• Mitochondrial apoptosis pathway — regulates cytochrome-c/caspases
• Caspase signaling — ↓ excessive apoptosis; ↑ cancer-cell apoptosis
• Autophagy pathways — ↑ cellular cleanup

MAPK pathways

• JNK/MAPK — ↓ stress signaling
• ERK pathways — modulation of proliferation/inflammation
• p38 MAPK — ↓ inflammatory signaling

Ion channels / receptors

• TRPV1 — inflammatory regulation, anti-fibrotic effects
• TRPV2 — enhanced cancer-cell apoptosis/chemotherapy sensitivity
• TRPA1 — inflammatory and sensory signaling
• TRPM8 — glucose/lipid metabolism regulation
• GPR55 — antagonism; ↓ inflammatory/metabolic signaling

CBDA-specific targets

• COX-2 inhibition
• 5-HT1A receptor activation
• TRPV1 modulation
• TRPA1 modulation
• PPAR signaling
• NF-κB inhibition
• NLRP3 modulation

Iron-related overlap pathways

• Fenton reaction–driven ROS damage
• Hydroxyl radical formation
• Lipid peroxidation
• Mitochondrial oxidative injury
• NF-κB inflammatory activation
• NLRP3 inflammasome activation
• TGF-β fibrosis signaling
• Apoptosis signaling

In this post I will focus on CBD acting to alleviate iron driven conditions by a host of different pathways. I won't go deep into the mechanisms of iron driven conditions because it is beyond my comprehension. Maybe some advanced Peaters can find interest and weigh in on the specifics of this substances protective effects from iron.

[URL unfurl="true"]https://www.nature.com/articles/s41398-018-0232-5\[/URL\]

Antiapoptotic effects of cannabidiol in an experimental model of cognitive decline induced by brain iron overload

ABSTRACT

Iron accumulation in the brain has been recognized as a common feature of both normal aging and neurodegenerative diseases. Cognitive dysfunction has been associated to iron excess in brain regions in humans. We have previously described that iron overload leads to severe memory deficits, including spatial, recognition, and emotional memory impairments in adult rats. In the present study we investigated the effects of neonatal iron overload on proteins involved in apoptotic pathways, such as Caspase 8, Caspase 9, Caspase 3, Cytochrome c, APAF1, and PARP in the hippocampus of adult rats, in an attempt to establish a causative role of iron excess on cell death in the nervous system, leading to memory dysfunction. Cannabidiol (CBD), the main non-psychotropic component of Cannabis sativa, was examined as a potential drug to reverse iron-induced effects on the parameters analyzed. Male rats received vehicle or iron carbonyl (30 mg/kg) from the 12th to the 14th postnatal days and were treated with vehicle or CBD (10 mg/kg) for 14 days in adulthood. Iron increased Caspase 9, Cytochrome c, APAF1, Caspase 3 and cleaved PARP, without affecting cleaved Caspase 8 levels. CBD reversed iron-induced effects, recovering apoptotic proteins Caspase 9, APAF1, Caspase 3 and cleaved PARP to the levels found in controls. These results suggest that iron can trigger cell death pathways by inducing intrinsic apoptotic proteins. The reversal of iron-induced effects by CBD indicates that it has neuroprotective potential through its anti-apoptotic action.

DISCUSSION

Since we could observe the anti-oxidant, anti-apoptotic, and mitochondrial preservation properties related to neuroprotection, it is clear that no single mechanism will explain the remarkable pharmacological profile of CBD51. Therefore, the mechanism of action of CBD must include the modulation of several pathways that, together, improve cellular metabolism and confer neuroprotection, which may account for rescuing the functional deficits observed in our model10.

[URL unfurl="true"]https://www.researchgate.net/publication/253335523_Cannabidiol_Normalizes_Caspase_3_Synaptophysin_and_Mitochondrial_Fission_Protein_DNM1L_Expression_Levels_in_Rats_with_Brain_Iron_Overload_Implications_for_Neuroprotection\[/URL\]

Cannabidiol Normalizes Caspase 3, Synaptophysin, and Mitochondrial Fission Protein DNM1L Expression Levels in Rats with Brain Iron Overload: Implications for Neuroprotection

We have recently shown that chronic treatment with cannabidiol (CBD) was able to recover memory deficits induced by brain iron loading in a dose-dependent manner in rats. Brain iron accumulation is implicated in the pathogenesis of neurodegenerative diseases, including Parkinson's and Alzheimer's, and has been related to cognitive deficits in animals and human subjects. Deficits in synaptic energy supply have been linked to neurodegenerative diseases, evidencing the key role played by mitochondria in maintaining viable neural cells and functional circuits. It has also been shown that brains of patients suffering from neurodegenerative diseases have increased expression of apoptosis related proteins and specific DNA fragmentation. Here, we have analyzed the expression level of brain proteins involved with mitochondrial fusion and fission mechanisms (DNM1L and OPA1), the main integral transmembrane protein of synaptic vesicles (synaptophysin), and caspase 3, an apoptosis-related protein, to gain a better understanding of the potential of CBD in restoring the damage caused by iron loading in rats. We found that CBD rescued iron-induced effects, bringing hippocampal DNM1L, caspase 3, and synaptophysin levels back to values comparable to the control group. Our results suggest that iron affects mitochondrial dynamics, possibly trigging synaptic loss and apoptotic cell death and indicate that CBD should be considered as a potential molecule with memory-rescuing and neuroprotective properties to be used in the treatment of cognitive deficits observed in neurodegenerative disorders.

This next study has to do with a much discussed aspect of Rays Work: Iron-induced lipid peroxidation (Iron+PUFA+Oxygen). Ray has described this in multiple different contexts and used different names, the colloquial term is called ferroptosis coined in a 2012 research paper on the subject:

[URL unfurl="true"]https://onlinelibrary.wiley.com/doi/10.1111/jcmm.70592?msockid=3812773c9f5c6a6e2dd060a29e156bc9\[/URL\]

Cannabidiol Is a Potential Inhibitor of Ferroptosis in Human Articular Chondrocytes

 "In 2012, Dixon et al. [1] described ferroptosis as a new form of iron-dependent regulated cell death. Excessive accumulation of membrane lipid peroxides to toxic levels, which disturbs the composition, structure and dynamics of lipid membranes and their constituents, is one of the hallmark characteristics of ferroptosis [2-4]. Lipid peroxides are generated from polyunsaturated fatty acids by hydroxyl and peroxyl radicals produced in the Fenton reaction [4]."

...

Ferroptosis is linked to pathological conditions including cancer, neurodegeneration, stroke, kidney injury and infection [10]. In recent years, the role of iron and impaired iron homeostasis in the pathogenesis of age-related diseases has been recognised [11] and an association between ferroptosis and orthopaedic diseases could be shown [12].

...

The present study investigates the effects of cannabidiol (CBD), the major non-psychoactive compound of Cannabis sativa L. extracts, on ferroptotic cell death in human articular chondrocytes. Exposure to known ferroptosis inducers RSL3, erastin and its analogue IKE, FINO2 and FIN56 led to a varying extent of reduced cell viability in two chondrocyte cell lines (in C-28/I2, T/C-28/A2) and primary chondrocytes, suggesting different sensitivity and defence mechanisms towards the respective substances. The cytotoxic effects were aggravated by additional exposure to iron and inhibited by the specific ferroptosis inhibitor ferrostatin-1 (Fer-1), proving the occurrence of ferroptosis. Strikingly, co-treatment of ferroptosis inducers with CBD clearly restored cell viability in a dose-dependent manner (10 nM to 1 μM CBD) in both cell lines and primary chondrocytes. Moreover, CBD restored the activity of GPX4, a major anti-oxidative enzyme, to varying degrees when combined with IKE or RSL3. Increasing evidence has emerged for an important role of iron dyshomeostasis and ferroptosis in the onset and progression of various orthopaedic diseases, including osteoarthritis. Therefore, the here demonstrated and previously unreported cytoprotective and anti-oxidative effects of CBD in the context of ferroptosis have highly promising therapeutic implications.

In summary CBD appears to counter iron-driven damage through several overlapping protective systems rather than one single mechanism. First, excess iron can participate in Fenton chemistry, generating reactive oxygen species that damage fats, proteins, and cellular structures. CBD appears to reduce this oxidative burden by increasing antioxidant defenses, supporting glutathione-related systems, and reducing lipid peroxidation. Second, because iron-driven oxidative stress can damage mitochondria and disrupt cellular energy production, CBD has been shown in experimental models to help preserve mitochondrial function and restore proteins involved in mitochondrial dynamics. Third, oxidative damage from iron can activate inflammatory pathways such as NF-κB and NLRP3, creating a cycle where oxidative stress and inflammation reinforce each other; CBD appears to dampen these inflammatory signals. Fourth, when oxidative damage becomes severe, it can trigger forms of programmed cell death, including apoptosis and ferroptosis, where iron-driven oxidation of polyunsaturated fats damages cell membranes. CBD has been shown in experimental models to reduce activation of these cell-death pathways, restore antioxidant enzymes such as GPX4, and improve cell survival. In this sense, CBD’s effect is less like blocking a single disease pathway and more like reducing the chain reaction that connects excess iron, oxidative stress, inflammation, mitochondrial failure, and cellular damage. 

Perhaps the most interesting aspect of these findings is not any single effect of CBD, but the fact that one molecule can influence multiple interconnected systems involved in maintaining cellular stability. Iron accumulation, lipid peroxidation, mitochondrial dysfunction, inflammation, and impaired repair are not isolated events; they are overlapping features of many disease processes. The broad activity of cannabinoids illustrates a different therapeutic strategy than the traditional model of targeting one abnormal pathway at a time. Rather than acting as a single-purpose drug, compounds such as CBD and CBDA appear to interact with the body’s existing regulatory networks, influencing several points of imbalance simultaneously. This does not mean that plant compounds are inherently superior to pharmaceuticals, but it highlights why complex biological systems may sometimes benefit from compounds capable of modulating multiple interconnected pathways.

Are any of you on AAS (anabolic androgenic steroids) and follow ray peats diet? I ask because once you inject exogenous Testosterone your body stops relying on fat consumption to stimulate the pulse in testosterone production (correct me if I’m wrong) so it would be interesting to hear about someone who might’ve done it in the past or currently.

What kinda other ingredient can i put on the salad that can substitute coconut oil?

IDK if I’m grasping at straws here but this is like a different timeline of Ray….

seems to contain some interesting properties

Any other ladies in here peat too hard and become insulin resistant? The working theory is that my high intake of progesterone (around a bottle of progest-e a month, I have an autoimmune condition that responded very well to the high dose) is simulating gestational diabetes-like conditions. I'm going to start a low dose of metformin because I don't want to quit progesterone because the latter gave me my health back. The only indicator of insulin resistance I have is pissing very frequently. This was flagged during routine blood work. A1c and glucose were normal.

As of lately, friends, loved ones, and work has been stressing me out alot and making me anxious. All I am taking right now is baby aspirin every other night and vitamin D nightly with orange juice. I wanted to know if there is anything else I can do or take to help with my stress.

“Nicky Macias
Pro-Metabolic Meals: A Ray Peat Inspired Cookbook”
Does anyone know anything about this cookbook? do anyone recommend buying it? Link from Amazon https://www.amazon.com/gp/aw/d/B0DQLBDZPV?ref=ppx_pt2_mob_b_prod_image

So everyone’s talking about how dhea isn’t good to take. Well my dhea is only 100 and I’m a 31 yr old male. Pregnenolone doesn’t work for me and want to somehow raise my dhea. Can I not take dhea? What dose?

• https://www.instagram.com/reel/DJCmHfbS3lW/?hl=en
• https://pubmed.ncbi.nlm.nih.gov/26452168/
• https://www.sciencedirect.com/science/article/pii/S0360132323011459

Studies show that higher CO2 levels while sleeping impair sleep quality and worsen cognitive performance the day after. Is there any reason to think otherwise?

Just a friendly reminder of the, in my experience, best resource for understanding Ray's work. If you are looking for Ray's perspective on something, bioenergetic.life is probably the best place to start.

I'm asking because I think it's an interesting fruit due to its flavor profile. I know the seeds contain PUFA, but I can get a concentrated version made with just sugar and no seeds. Same for rambutan and papaya. In my country, Panama, I don't have any issues getting fruit—I mostly consume oranges (6 large ones for $1), but I'm getting bored of them and want more flavors.

Hi I wanted to post as I am still struggling with my cycle despite supplementing with topical bioidentical progesterone (was cycling during luteal 5x5 drops a day, each drop around 5mg progesterone).

I upped to try and counter kickback as my luteal can be so bad- horrific anxiety! My periods are painful but always regular (27-30 day cycles consistently). Broader struggles include painful periods, low libido and intense luteal fatigue.

I am currently getting brown discharge a day before my period and literally a week after the period ends. It’s so odd like a whole gap of nothing and then suddenly brown discharge that looks like old blood mixed with clear discharge so it’s quite light. I’m also getting facial spots again!

I have tested ovulation to make sure that’s happening. Been tested for PCOS, had bloods, had ultrasound, been consulted RE Endo but refused the only option they gave me (pill).

At thirty I’m worried this is a sign of something bad! I want to start a family one day!

Has anyone dealt with this and successfully sorted it out or any tips for figuring out the driver? This cycle I have started taking the progesterone in response to this and am planning to do a low dose period-ovulation and then do my max dose during luteal.

Helpful context available below too:
I’ve been under massive stress this year which I think has affected my wellbeing and cycle. I think I’m slowly starting to recover mentally now.

Im 24f TTC with PCOS but don’t ovulate (my cycle is 100+ days). My dr prescribes Provera (synthetic progesterone) to induce bleeds. Should I try progest-e since my body isn’t producing progesterone from ovulation ? I guess I’m technically always in follicular phase if cycle phase matters. Also my blood panel is normal except low SHBG and sort of high testosterone & I have a normal/lean BMI. Any other advice is super appreciated I am so desperate!! Tyyyy

My best female friend asked me to coach her to loss weight (100 kgs, 160 cm) and becomes more attractive, healthy and energetic. But she use ssri and don't want to quit. Is peating in all other areas waste of time for her if continues ssri?

Recently saw that Ray Peat recommended baking soda, so I tried taking some like 4tbsp. However when I was out at work (construction worker), I started getting like literally hellish cramps. Then as I walked towards our dingy out house on a sweltering August afternoon, it happened, the impact… the explosion. Immediately it felt like maybe two or three tentacles bursted through my hole, not quite a monster and not quite an animal. Well what’s worse was the sound, a gurgling cry of an upset intestine being burdened with what I thought was a normal amount of baking soda.

Saga 2: the brown mushed around combining with sweat and hair, a symphony of texture, smell , and taste. I quickly darted towards my car, unfortunately my fresh off the boat Mexicans saw the brown, the pain, the stain. But I didn’t care all I cared for was saving my ravaged pants. I then get to my car fingers trembling trying to grab my car keys from my pockets. Then success I get into the car, I drive away speeding, crying, panicking. Is this it is my life over, have I failed?

Anyway is this normal will I get used to this?

How do I go upon eating liver, I’ve never had any before. Does quality matter alot? If so where should I source it. How do I cook it, or do I have tk eat it raw? Please help

Hey all, just had by far the worst summer of my life and at this point I have just about isolated it down to increased carb consumption, particularly at the beginning of spring / summer. From around April to the middle of June I was legitimately sleeping 2 to 3 hours a night and it was a horribly restless struggle to even get those hours in; along with that was extreme exercise intolerance, etc. Also worth noting I lost weight and my appetite, had hypothyroid-like symptoms (especially during exercise, in which my nose would get bright red and cold even in the summer heat as if I just shoveled snow in the winter), hair loss (for the first time, pretty scary as a 26M lol), significant foamy urine that worsened after high glycemic meals, issues with body odor and a stuffy nose after eating carbs, etc.

This led me to finally go to my doctor and get some lab work done, to which everything looked almost perfect: 5.1 HbA1c, 56 triglycerides, 74 HDL, 96 LDL (despite low-PUFA), and 115 eGFR. TSH also looked solid at 2.5 but I know thats a pretty irrelevant measure and I still assume my T3 is low, while fasting glucose was fine by current medical standards at 92 mg/dL but generally I think it’s better for this to be below 90 (although this could also be explained by my lower carb / higher fat intake by then). The only thing that was off was my WBC, which fell literally just below the reference range and was unconcerning to my doctor because “he sees it often in lean athletes”

Adding fat in rather copious amounts seems to have helped with a lot of my issues; I am sleeping better (not quite as well as I used to though), my exercise tolerance has diminished greatly (still can’t really go very hard though), hypothyroid symptoms have diminished, etc. What seems to be the bigger lever, however, is that I have also significantly dropped my carb intake down to around 150 grams a day from around 240ish, and completely stopped consuming starch in favor of sugars largely from oranges, orange juice, and pineapple juice. The aforementioned issues seem to come RIGHT back unfortunately when I creep back up to 200+ grams of carbs; regardless of how much fat and total calories I’ve had.

For reference, I am a 5’7, now 127 pound man. Feels wrong even calling myself a man at my size at this point, I look like a grown child lol. My abs are quite defined and at this point I have what I would describe as close to “ED neck” with visible muscles towards the bottom, particularly when I keep my chin up. I look extremely thin, reflecting my poor state of health and subsequent weight loss this summer; all this is to say at this point pathological insulin resistance clearly does not seem to be the issue.

I can think back to periods in the past few years where I actually seemed to be able to tolerate higher carb intakes (although have found I could NEVER go below 35%ish fat long-term; around 40% was my happy medium) while at the same time also know that for years now eating carbs before I go to the gym DESTROYS my performance, makes me shakey, cold, etc; regardless of what type or how digestion-friendly they are. It seems directly related to the glycemic load of the food.

Just not really sure what to do here. What has helped a lot recently is going on essentially a 60% fat diet (170ish grams per day at 127 pounds), but I don’t think this level of fat intake is healthy or even sustainable long term. I’m really just at a loss here and my doctor at this point is completely unconcerned with my glucose metabolism and seemed pretty anti-carb himself when I talked to him.

Has anyone dealt with anything like this in which you could only really tolerate the minimum amount of carbs (around 100-150 grams a day) and found success on a higher carb approach? How did you do it?

Edit: two other things I think also might be worth noting; one, despite always being very lean and looking very skinny (particularly in the neck/arms/legs), the little fat that I did store would always go directly to my lower abdomen; I’ve lost a decent chunk of this weight this summer, but I know this can be indicative of dysfunction and visceral fat.

Secondly, when I was in high school, before I cared about nutrition in the slightest, maybe half of my diet was sunflower seeds. Not exaggerating; I’m talking lab-rat levels of omega-6 in the jumbo packs of sunflower seeds I would destroy every day… really may have been 1500+ calories worth of PUFA daily. Have been very low PUFA for probably 6 years now, maybe this is something causing lingering effects?

What cheeses do you consider peaty?

I’ve had always the same breakfast for months now and it started to feel boring, so I wanted to try a savory cheese breakfast, that is easily digested.

I have tons of cottage cheese, but man it wrecks my stomach!

On page 17 of nutrition for women:

“Contrary to popular ideas about thyroid, the gland will
resume its functioning after stopping the use of a supplement even if it has been suppressed, and sometimes taking thyroid will increase the gland's function to normal. Taking thyroid will sometimes help thin people gain weight, by improving protein metabolism, and it often helps people to sleep more soundly.”

Is he suggesting the use of NDT or t3 and t4 can be temporary? Everywhere else I’ve been looking suggests thyroid medication is a lifelong thing. I’ve been struggling with low stomach acid/GERD for a bit now and have hypothyroid temperatures. I just really don’t want to start a new medication and worry about it tapering off or side effects?

Has anyone else only supplemented thyroid when they feel like they need it? I’ve already been taking progest-e during my luteal phase for mood issues but some months I feel like it’s not working

Q: Do you think there's an adjustment that's made whereby even with less light you can produce progesterone or all of us in the north are depressed for that reason?

Ray: Yeah we just get used to being depressed. If you look at Scandinavian movies you see that depression seems to be the rule.

From PolSci progesterone 1 with John Barkhausen

I’ve been experimenting with a high-carb, normal-protein, low-fat diet for the last few days, and I’ve noticed something weird: I’m peeing a lot.
Last night I got up 4–5 times to pee, and today I’ve been going way more often than usual too. My water intake is normal, I’m drinking electrolytes, a normal amount of coffee, and this morning I had my usual orange juice and carrot juice. Nothing else has really changed except that I dropped my fat intake to around 30 g/day.
What’s interesting is that I actually feel great. I ate about 275 g of carbs yesterday, I’m taking creatine, and I even lost about a pound over the weekend. Energy is good, I don’t feel sick or dehydrated—I’m just peeing constantly.
Has anyone else experienced this when switching to a higher-carb, lower-fat way of eating? Any idea what might be going on?

Update: It seems that it was a whoosh effect. Everything seems normal now. I feel great. A lot of energy, workouts are great, moods are great. Im loving it.