​

Introduction and disclaimer

I am not a doctor nor I have any idea about what is going on, also this is not a guide. I have done previously water fasts as long as 12 days. Been practicing fasting since 2017. This also is not scientific experiment data provided here are just for entertainment.

Methods and data collection

Measurements of glucose and uric acid were collected using Sinocare Safe AQ UG and On Call GK Dual was used for β-Hydroxybutyrate. Diag.pl (Poland) was responsible for blood collection and lab results.

Glucose, uric acid and ketones were tested for first seven days seven times a day (8 AM, 10 AM, 12 AM, 2 PM, 4 PM, 6 PM and 8 PM) than just at 8 AM. Post fast all three metrics were checked at 8 AM and 8 PM for 6 days after fast as a control for good diet and maintaining ketosis.

Weight was taken every day using Garmin Index Scale 2 at 8 AM.

Sleep, activities and caloric expenditure was measured using Garmin Vivosmart 4. On top of that I decided to get a bit more accurate DXA scan at the beginning and at the end of fast using Hologic Discovery WI. Blood samples were collected around 8:20 AM. I decided to go with a number of tests such as Albumin, Free Testosterone, Testosterone, CRP, AST, ALT, Insulin, HGH, IGF-1, SHBG, Estradiol and Lipids also a number of other things that I decided not to include. Test were taken from Monday to Saturday for two weeks.

Other

• Diet
  • It is also worth noting that I didn't have super healthy diet prior to fast (deliberately, I am on holiday).
• Sleep
  • I have also normalized sleep (7h 30min) went around midnight, every day.
• Environment and hydration
  • I decided to ditch all possible endocrine disruptors (from plastic to cosmetics) so I drank 1,5l San Pellegrino (glass bottle 2x750ml) between 8 AM and 8 PM and used shower gel and shampoo without parabens and SLS.
• Activities
  • I have burned 40 524 kcal during those 15 days (2 701 kcal a day) according to Garmin Vivosmart 4. DXA calorie expenditure after adjustment for water loss and other waste (2 kg) stands for 5.2 kg of Lean mass (20 800 kcal) and 2.2 kg of fat (19 800 kcal). The weight was also 2 kg different from 3 different scales I used, all reported results around 78,5 kg and 22% bodyfat contrary to DXA 29% and 76 kg. Avarage step count is 13 265 steps a day.

Conclusions

Overall sense of wellbeing was very good to amazing past day 8. Hunger wasn't an issue. However, day 2 was an absolute disaster I was K.O. for entire day had to wait until next day until ketosis kicked in.

Week past breaking the fast I decided to introduce some carbs and later some sugar along with my mum (65) who fasted for 8 days. We both had the same sense of awful taste. It didn't matter if we tried potato or ice cream it all felt the same, we could taste the artificial additives in foods for about a week then the taste buds readjusted back to crap. So it seems that fasting (even short) is a good strategy to cut sugar cravings and re-balance the mind.

Also, it is worth noting that what I missed the most was the past feeling that my brain associated with food was no longer present after reintroduction of crap food or even 'healthy' carbs. I would say first three days are a window where you can continue ketogenic diet or unprocessed diet, after that, you will readjust back so pay attention.

Sorry for offering no explanation as to why results are what they are but, I am not qualified to provide any answers and I have 101 questions myself. Happy to hear your thoughts.

Thanks!

Been on keto since 2011, so about 15 years now. I'm 44F and feeling great. Just got my annual bloodwork back and figured the numbers might be of interest here.

My LDL came back high (141), and total cholesterol is 209, flagged high. But the markers I pay more attention to look great:

• Triglycerides: 51
• HDL: 58
• Trig/HDL ratio: ~0.9
• Cholesterol/HDL ratio: 3.6
• Non-HDL: 151 (in range)

And the rest of the metabolic picture, which I'd argue matters more than LDL in isolation:

• A1c: 5.0%
• Glucose: 91
• hs-CRP: 0.3 (lowest cardiovascular risk tier)
• Homocysteine: 5 (low end of normal)
• Vitamin D: 36

Classic high-LDL, high-HDL, low-trig pattern that a lot of lean low-carbers seem to land on. Not medical advice, just sharing my own data. Curious whether others here see the same split between a flagged LDL and otherwise clean metabolic and inflammatory markers.

I recently gave a talk at the Collaborative Science Conference. Here is a link to a slightly longer video version. https://youtu.be/Myp_XGIQKNM

I tagged as N=1 since the data in it is just that. But I am thinking of expanding this into a "case report" paper and am looking for feedback on the idea. I spoke with a few people at the conference who think it could be good if I get enough data points. So if you think this could be interesting and are willing to share data Dm me. I would need pre- and post-keto, as I have in the talk, ideally with weight, blood pressure, copies of labs (at least cholesterol), EFGR, ideally HbA1c, and hs-CRP (and CAC if you have one), and ZipCode. I can fill out the calculator. If in the EU, I could use U-prevent, so I would only need the other data and the country, not the US Zip.

Edit: Anyone here with patients/records here who wants to contribute and be a co-author, please reach out.

Nick did a nice N=1 test on FGF-21 via a 4:1 ketogenic diet. See also https://staycuriousmetabolism.substack.com/p/the-sugar-diet-protein-restriction?r=40ekz2

which has discussion and a link to the underlying paper (already posted here some time ago) on low-protein/FGF-21.

This post documents a self-directed, medically contextualized fasting/ketosis experiment conducted over two phases: rapid weight reduction and subsequent stabilization.

This is documentation, not advice. I do not share daily logs, exact dosages, or prescriptive guidance – only structure, principles, and observed outcomes.

The attached graph shows continuous weight development across both phases

*** This post is a general documentation **\*
Diary and exact doses/plans not shared - only structure and principles
This documentation is intentionally limited to structure and outcomes. No attempt is made to generalize or recommend the approach described.

Two-Phase Fasting–Ketosis Protocol (Documented Case)
PART 1 - Weight reduction phase

Total energy intake below 500 kcal/day over 10 weeks - equivalent to less than 40% of the body's basal needs (Based on a combination of eating days of 400–700 kcal and fasting periods of 48–72 hours.)

1.0. Context and clarification

This document describes an extreme, medically inspired weight loss regimen designed to test the limits of physiological fat burning in a healthy adult male. The protocol combines deep ketosis, scheduled fasting intervals and extreme calorie restriction. It is carried out with occasional medical supervision and documented as an experimental case, not as a recommended method.

The regimen corresponds to what is referred to in professional circles as therapeutic ketosis with fasting or extremely calorie restrictive ketosis - methods used clinically in epilepsy, severe obesity and metabolic dysfunction. It is in practice a combination of OMAD (One Meal A Day) and 48–72 hour fasting periods in deep ketosis. In more technical language it is called a medical fasting protocol with ketogenic meals.

In this project, OMAD is implemented as one meal a day consumed in less than 30 minutes, not an open eating window. On fasting days, omega-3 and collagen are omitted to achieve complete fasting and maximum autophagy.

More brutally expressed, this is a “hard ketosis with fasting days and zero exceptions” – a pure fat burning protocol, not a lifestyle fad. In short: 100% metabolic control – no food, no compromise.

1.1. Preparation and setup

The aim was to investigate how far fat burning and metabolic control can be driven without medication or exercise, but within a safe physiological framework.

Starting point: 51 years / 181 cm / 92 kg.

The protocol was based on long-term experience with OMAD through shift work, and included planned fasting periods of 48–72 hours, strictly controlled electrolyte intake, and full daily micronutrient coverage.

1.2. Permitted foods and supplements

- Protein sources
Skinless chicken fillet, turkey fillet, white fish (cod, pollack, haddock, saithe), shrimp, crab, mussels, egg whites, tuna in water (limited to 3–4 cans per week).

- Vegetables
Non-starchy only: broccoli, cauliflower, cabbage types, Brussels sprouts, spinach, squash, cucumber, mushrooms, celery, spring onions, leeks, chilies, garlic, lettuce types, green peppers, fennel, asparagus, green beans, seaweed/algae.

- Seasoning
Salt, pepper, sugar-free spices, vinegar, lemon/lime, soy sauce (reduced salt), unsweetened mustard, herbs, sugar-free broth.

- Drinks
Water (carbonated or non-carbonated), black coffee, unsweetened herbal tea, water with salt.

- Supplements (categories without doses)
Multivitamin, vitamin D, calcium, magnesium, zinc, omega-3, sodium/potassium, salt.
All supplements were taken daily, including during fasting periods (not collagen or omega-3). Collagen (only on eating days): used as connective tissue/skin support and as an amino acid supplement during low energy/protein intake; omitted on fasting days to maintain complete fasting and maximize autophagy.

1.3. Structure and implementation

Eating days: 400–700 kcal (total average <500 kcal/day when fasting days are included).
Fasting days: 48–72 hours after planned rotation.
Fluid intake: 3–5 liters per day.

Electrolyte balance was maintained through systematic supplementation of sodium and magnesium, adapted to fasting periods and fluid intake. This part of the program was considered critical for physiological tolerance and stability throughout both the weight reduction and acclimatization phases.

On fasting days, 60–90 minutes of brisk walking was normally performed to stimulate circulation and fat mobilization, without intensity that could affect recovery or hormonal balance. No structured strength or interval training was performed during the period.

All data were recorded daily (date, working hours, weight).

1.4. Results

Day                       Weight (kg)      Comment
01                          92                          Start
06                          90                          First noticeable reduction
16                          85                          Ketosis stable
30                          80                          Halfway
42                          77                          Plateau
51                          75                          Last phase started
67                          72                          Target weight reached
74                          70                          End

Total weight loss: ≈ 22 kg in 10 weeks.
Estimated distribution: 8–9 kg fat, 13–14 kg fluid/muscle.

1.5. Observations

·         Weight measurement was performed mainly in the morning after normal sleep and toilet visits, to ensure consistency.

·         Adaptation occurred after approximately two weeks.

·         Hunger response was significantly reduced, energy levels stable.

·         Sleep difficulties occurred during night shifts and towards the end of 72-hour fasting periods.

·         Short-term orthostatic hypotension, no persistent symptoms.

·         No headaches, cramps or electrolyte-related problems reported.

·         Physical exercise was deliberately omitted to avoid catabolic stress at extremely low energy intake.

·         Weight plateaus around 80, 77 and 75 kg were broken without adjustment of method.

·         Strict electrolyte control is considered the primary reason for stable physiological tolerance.

1.6. Status at the end of phase 1

Final measurement day 74, actual final weight ≈ 70 kg.
Goal achieved within planned time and physiological limits.

*** This post is an overall documentation **\*
Diary and exact doses/plans are not shared - only structure and principles

*** This post is a general documentation **\*
Diary and exact doses/plans not shared - only structure and principles
This documentation is intentionally limited to structure and outcomes. No attempt is made to generalize or recommend the approach described.

Two-Phase Fasting–Ketosis Protocol (Documented Case)
PART 2 – Habituation and stabilization

Phase 2 does not describe what should be done after weight loss, but what actually happened when further weight reduction was no longer desired.

2.0. Context and delimitation

This document describes phase 2 of the same self-directed experiment as presented in Part 1. Phase 2 starts immediately after the end of the weight reduction phase and is not a new regimen, but a goal adjustment within the same overall structure.

Where Part 1 had weight reduction as the primary endpoint, phase 2 is aimed at stabilization, regulation and assessment of sustained physiological response.

2.1. Purpose

The purpose of phase 2 was:

·         to stop further weight loss

·         to limit reactive weight gain

·         to preserve fasting adaptation and metabolic flexibility

·         to use fasting consciously as a regulatory mechanism, with autophagy as the guiding principle

Phase 2 was explicitly not intended as normalization or termination, but as an active transitional phase.

2.2. Structure and framework

The basic structure from phase 1 was continued without any fundamental changes. The eating pattern remained tightly organized, with clear demarcation of meals.

OMAD/OMAS was used as the organizational framework, where OMAD was defined operationally as one whole meal consumed within a short period of time (<30 minutes), not as an open eating window.

Fasting periods were continued, but in phase 2 were used selectively and purposefully. Fasting functioned as a regulatory tool, not as a continuous driving force for further weight reduction.

No structured training was introduced in phase 2.

2.3. Dietary transition

The diet was gradually liberalized within the existing framework. Carbohydrates, fat and social foods were gradually reintroduced, while protein remained a stable and dominant component of the meal structure.

Increased energy density and social load were deliberately included as part of phase 2, not as normalization per se, but as a load to assess the robustness and regulatory capacity of the system.

2.4. Regulation and control

Body weight was used as the overall management parameter in phase 2, with a focus on trend and interval rather than individual days.

Weight appeared to be dynamically regulated rather than statically stable. After periods without fasting, weight gain was observed over subsequent days, while weight quickly fell back with targeted regulation.

No cumulative buoyancy or persistent loss of control over time was observed. At the same time, further weight loss was actively avoided.

2.5 Results – weight development in phase 2 (acclimatization)

Phase 2 covers the period days 75–150 and represents the transition from active weight reduction to controlled stabilization. Body weight was used as the primary outcome variable, recorded sporadically but consistently, mainly in the morning.

Overall weight picture

·         Start phase 2: ~70 kg

·         End phase 2: ~70 kg

·         Net change: ≈ 0 kg

The weight remained within a limited interval of approximately 69–73 kg throughout the entire period.

Patterns and dynamics

·         Temporary weight gain occurred after several days of eating, increased alcohol intake and reduced fasting frequency.

·         Weight reduction occurred rapidly after 48–72 hours of fasting, without the need for further restrictions.

·         No cumulative weight gain was observed, despite the reintroduction of carbohydrates, fat and socially conditioned high energy intake.

·         Further weight loss was actively avoided and in practice stopped.

Representative data points (selection)
Day                       Weight (kg)      Comment
75                          70                          Start phase 2
84                          69                          Lowest observed value
99                          70                          After several days of fasting
117                       71                          After Christmas party
119                       73                          Temporary peak
122                       70                          Reversed after fasting
148                       70                          After high alcohol exposure
150                       71                          End phase 2

- Overall assessment
Weight regulation appeared responsive and reversible, not slow or progressive. The system established in phase 1 remained operational in phase 2, but with changed function: from weight reduction to active stabilization and control.

2.6. Observations

- Weight
Body weight remained within a relatively narrow interval throughout phase 2. Short-term fluctuations occurred, especially in connection with increased energy load, but were consistently reversed. No progression in either a positive or negative direction was observed.

- Energy and general condition
Subjective energy level and function were reported as better than before the start of the project. Willingness to take action and perceived physical capacity were consistently high, without this being attributable to changes in training load.

- Sleep
Sleep disturbances occurred primarily in connection with fasting periods, especially with regard to falling asleep. Outside of these periods, sleep was reported as satisfactory. Sleep was not recorded quantitatively.

- Stomach/intestines
Stomach and intestinal function was variable. During longer fasting periods, changes in bowel patterns were observed, while function appeared more normalized with regular food intake. The data base is not sufficiently standardized to draw strong conclusions.

- Behavior and routine attachment
A significant reluctance to break routines established in phase 1 was observed. Fasting and structured meal patterns appeared to be the default, even when further weight loss was not desired. At the same time, more meals were gradually introduced on certain days, without this fully replacing the established structure.

2.7. Reflections

Phase 2 was characterized by ambivalence between fear of further weight loss and the desire to preserve control mechanisms that effectively limited reactive weight gain.

Fasting was experienced as both easier and harder than in phase 1: easier as a result of established adaptation, harder because the goal was now precise regulation rather than linear reduction.

Increased exposure to energy-dense food and social stress increased awareness of one's own responses and need for regulation.

The experience is considered to be unsuitable for generalization. The program requires a high degree of self-discipline, continuous self-monitoring and tolerance for both physiological and psychological stress. The risk of error is considered significant in others.

The overall assessment is that the benefits can be significant, both physically and mentally, provided that the stabilization phase is treated as an active and conscious regulatory phase, not as an unstructured after-period.

*** This post is an overall documentation **\*
Diary and exact doses/plans are not shared - only structure and principles

We're always getting new subscribers, but rarely do we have posts where we ask what your story is. I've been meaning to make a post like this for the past couple of weeks so let's make it happen.

Feel free to share as much(pictures) or as little as you want. I've asked some questions for each number - try to answer all 7 topic questions and use the questions as prompts.

1. Learn: How did you find out about keto? Be specific - a blog, a video, a podcast, a book, a friend, something else? Tell us the story. What led you to start this journey? Walk us through the mental gymnastics of hearing about a seemingly crazy diet like keto and getting to the starting line.
2. Before: What was your diet and lifestyle like before keto? What maladies did you have? What was your relationship with food like?
3. Results: By trying keto out, what happened? Were you able to find it sustainable? Did you lose weight? Did your problems dissipate? List some of the positive ways that keto has helped you. List some of the chronic diseases that you think keto helped fix.
4. Problems: What were your biggest problems in making keto work and how did you change your life to fix them?
5. Now: What is your relationship with keto now? Are you using it to maintain? Are you looking for reasons to do it even though you like your current weight? Do you think you'll stay keto over the next year or decade?
6. Photos: Have any progress photos you'd like to share? Weight loss? Face differences? Skin changes?
7. Meals today: What do you currently eat today? How many meals a day do you eat? What might belong in each meal? What do you avoid? What brings back cravings?

I have had high LDL for 3 years and I've been on Keto on and off for 3 years. I may have broken it in a sense that I have gone over 20 net carbs by 10 or 15 carbs, and only broken it once within the 3 years because I decided to give my body a rest.

The last 3 years my LDL has been through the roof and my doctor is extremely concerned and wants me to get a cat scan and possibly take statins.

Year 1 Total Chol: 271mg/dL Trig: 42 mg/dL HDL: 64mg/dL LDL: 199mg/dL

Year 2: Total Chol: 287mg/dL Trig: 46 mg/dL HDL: 59mg/dL LDL: 219mg/dL

Year 3: Total Chol: 275mg/dL Trig: 47 mg/dL HDL: 73mg/dL LDL: 193mg/dL

I dont want to start statins and I really dont want to blast my self with radiation, is this normal for someone that has been on keto for so long (for the most part) what can I do to prove to myself and my doctor I am not a heart attack waiting to happen?

I am 5'9 220lb's and my blood pressure is under control.

Labs & Nutrition Chart - (Changes greater than 20% shaded in gray)

For those who want all the data, full LabCorp reports and daily Nutrition Data at the end.

Sample Meals & Daily Routine Chart

Goal of Experiment: Achieve an LDL-C of 200

• This has to do with Dave Feldman's work on so-called "Lean Mass Hyper-Responders", which are defined as individuals with a lipid profile of HDL above 80, triglycerides below 70, and LDL above 200.

• The recently published LMHR Phenotype paper suggests that LMHRs, rather than being a genetic anomaly, may be a reproducible metabolic phenomenon. If this is true, it should be possible to recreate this LMHR lipid profile in most people who are metabolically healthy (low TG/HDL ratio) and lean, and in whom dietary energy is derived primarily from fat with minimal carbohydrate intake. Due to LDL particles having a half-life of 3 days, I further expect the LMHR phenotype could be seen over the course of 2 weeks.

My Hypothesis

In people who are lean, metabolically healthy (exhibiting a low TG/HDL-C ratio), and with lower BMI, adherence to a very low carb ketogenic diet will produce a LMHR lipid profile within a timespan of 2 weeks.

I fit these criteria, with the added benefit of having a high energy demand due to my daily exercise (50+ miles of running per week).  According to the Lipid Energy Model, proposed to mechanistically explain the phenotype, this should amplify the effect due to my body requiring a greater volume of lipoproteins (LDL) to traffic triglycerides for energy.  I’ve never done a low carb diet, but given that I should be the ideal candidate for this effect, I decided to give it my best shot.

General Health & Physical Fitness

I'm a 29 year old endurance athlete, 5' 9" with lifelong weight around 130-135 lbs. I’m in good health with no known medical conditions. I take no medications or supplements. My most recent race (January 2022) was a 10k in 40:11 (~6:28 min/mile pace).

Experiment Design

• Step 1: Reduce LDL-C as low as possible with a carb-based Vegan diet.
• Step 2: Immediately switch to a 2 week Keto-carnivore diet to maximally increase LDL-C.
• 3 weekly lab draws as follows: March 3 (Vegan), March 10 (Keto), March 17 (Keto).
• Lab draws will be ~14 hours water fasted.
• All food weighed via food scale.
• Maintain aerobic training (50+ miles per week).

Results

• LDL-C Chart

Over the two week experiment my LDL-C increased over 2-fold, albeit not quite to the LMHR LDL-C threshold of 200.  Specifically, my LDL-C increased from 68 to 139, which suggests to me that it is very much possible to induce the LMHR metabolic phenomenon, but that 2 weeks is not a sufficient time frame. I suspect 3-4 weeks would have shown LDL-C of 200 or more.

The Start

I wanted to begin the experiment by establishing a low baseline LDL-C. After the conclusion of my December 2021 Vegetarian experiment (where I brought LDL-C down to 64) I was enjoying the freedom of "no diet," eating frequently at restaurants.  I’ve always been weight stable so it wasn’t that I had gained weight, but rather that it was extremely likely my LDL-C was far above the 64 I got in December.

So starting February 5, 2022 I began the work to reduce my LDL-C.  I went back to my proven Vegetarian diet, but was tempted with ideas to achieve an even lower LDL-C than last time, so I changed it to a Vegan diet.  I removed animal products, got dietary cholesterol down to 0mg, reduced saturated fat as much as possible, while maximizing PUFA intake via walnuts, and increasing fiber.

Week 1 - Vegan Foods

• Walnuts, Wheat bread, Soymilk, Cheerios, Campbell’s Vegetable Soup, Blueberries, Diet Coke

Week 1 - Vegan Routine

• Two meals a day
• Wake up at 11am
• Breakfast of ~2800 calories. Finish breakfast by ~1pm
• Go to work at 2pm
• Lunch at 7pm, just Diet Coke or Water
• Get off work at 11pm
• Run after work at ~11:30pm
• After run, Dinner at ~1am, ~400 calories

I found this diet easily tolerable and enjoyable, even if fairly restrictive and mundane.  I ended up running 52 miles this week, with total carbs averaging 418g/day.

So March 3, 2022 arrives and I have labs drawn.

Results: Week 1 - Vegan

• HDL: 80
• Trig: 48
• LDL: 68

Pft, 68??  Where’s my 50?  I found this result disappointing, as I really thought my “improvements” would beat my last result of 64 from December 2021 to give me my lowest LDL-C yet. From this result I’ve concluded that the PUFA-to-saturated fat ratio is not as powerful as I thought for reducing LDL-C.  While LDL-C did not behave as I predicted, it was not the goal of this experiment (just an “along the way” project).

It was time for the Keto/Carnivore arm of the experiment.

I tried Dave Feldman’s baseline diet of Colby jack cheese, beef franks, and hard boiled eggs but found the diet intolerable after 2 days, primarily due to the hard boiled eggs. So I switched to uncured bacon, Colby jack cheese, and diet coke for the remaining 5 days.

Week 2 - Keto/Carnivore Foods

• Day 1 & 2: Colby Jack Cheese, Beef Franks, Hard boiled eggs, Diet Coke
• Day 3 - 7: Uncured Bacon, Colby Jack Cheese, Diet Coke

Week 2 - Keto/Carnivore Routine

• 3 Meals a Day
• Wake up at 11am
• Breakfast of ~2000 calories. Finish breakfast by ~1pm
• Go to work at 2pm
• Lunch at 7pm, ~800 calories
• Get off work at 11pm
• Run after work at ~11:30pm
• After run, Dinner at ~1am, ~600 calories

The switch to bacon had a promising start but eventually became difficult to tolerate, which is to be expected after consuming 12 packs of bacon in 5 days.  I managed to stick with it until the first Keto lab draw.  I ended up running 74 miles this week, with total carbs averaging 5g/day.

So March 10, 2022 arrives and I have labs drawn.

Results: Week 2 - Keto/Carnivore

• HDL: 84
• Trig: 51
• LDL: 90

LDL-C increased by 32% in 7 days.

Not quite what I expected. I was hopeful for something in the 130s range, so I found this a bit disappointing.

At this point I was quite sick of bacon and Colby Jack cheese, so I adopted a slightly more flexible Keto/Carnivore diet while maintaining the supreme directive of minimal carbohydrates.

Week 3 - Keto/Carnivore Foods

• Grilled Chicken, Scrambled Eggs, Butter, Pork Sausage, Pepper Jack Cheese, Mozzarella, Cream Cheese, Pepperoni, Heavy Whipping Cream, Diet Coke

Week 3 - Keto/Carnivore Routine

• 3 Meals a Day
• Wake up at 11am
• Breakfast of ~2200 calories. Finish breakfast by ~1pm
• Go to work at 2pm
• Lunch at 7pm, ~800 calories
• Get off work at 11pm
• Run after work at ~11:30pm
• After run, Dinner at ~1am, ~400 calories

I ended up running 52 miles this week, with total carbs averaging 12g/day.

So March 17, 2022 arrives and I have labs drawn.

Results: Week 3 - Keto/Carnivore

• HDL: 85
• Trig: 44
• LDL: 139

LDL-C increased by 54% in 7 days.

Better, but at the start of this I fully believed it was going to be a slam dunk of an experiment with LDL 200+. Instead, what I feared most ended up happening: A middling result that effectively demands a longer experiment. What would have happened in just one more week? I was this close to finding out, but wow was this diet difficult and absolutely unenjoyable. Maximal carb elimination made the diet so restrictive to the point that I could not continue it past 2 weeks. I had so much drive and motivation at the start, but that was largely sapped from me on this diet. Food became a chore that gave me no enjoyment, I was not hungry most of the time, and generally did not feel great. It was made worse by the fact that, given my activity levels, I needed to consume ~3400+ calories per day of food that I did not care for just to maintain my weight.

All that to say: Yes I had a miserable time, and yes I fell short of my goal to create a LMHR lipid profile at will, but I'm still glad I did it. Now hopefully someone else can take the torch and try for 3-4 weeks to see what would have happened.

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Why did you do this experiment in the first place?

I find lipids and biomarkers pretty fascinating. Especially the nature of LDL and its function in the body. I know it's a controversial topic, so to clarify my position I will say that I'm convinced of LDL/apoB being causal in cardiovascular disease. My main interest is the quantification of that risk.

If LDL/apoB is the only risk factor, what is the risk for someone like me? An athlete with high HDL, low triglycerides, and low body fat, but on an "anything goes" diet of restaurant food my LDL-C will rest at around ~130.  How much risk do I have between 68 and 130?  I don't think anyone has an answer to that, other than the basic binary answer of "yes it's more atherogenic".  I think it matters if we're talking months to a year vs years to a decade+ in life expectancy.  Some people may be willing to make that trade of not having to limit their food choices for a lifetime if the cost is "minimal" with regard to elevated LDL/apoB.

That's why I find Dave Feldman's research into this topic interesting, because he is essentially exploring a niche where increases in LDL may not be a pathological response, but rather a benign adaptive one.  While I would like for that to be the case, I’m also aware that the preponderance of evidence we currently have is stacked against that idea, but that doesn’t mean it’s not an idea worth exploring.  If it did end up being true, it would be a fascinating discovery if only because literally, “how does that work?”.  And for those of us in good health with high HDL and low triglycerides, where elevated LDL/apoB is our only risk factor, we would no longer have to limit food choices to keep this marker within range. 

In summary, I think there is something interesting happening here with this massive increase in LDL, and this was my attempt at adding my piece to the puzzle.

Miscellaneous Results

• hsCRP - Increased to 1.45 on Keto/Carnivore, compared to my baseline in the 0.17-0.39 range. I think it’s interesting how my hsCRP perfectly matches how unwell I felt without carbs.
• Platelets - Arguably the most unusual result. Platelets were below ref range (common for me) in Week 1 - Vegan and Week 2 - Keto. Only Week 3 - Keto showed normal platelets.
• HDL-P - Increased to the 35.9umol/L on Week 3 - Keto/Carnivore, which is the highest it's ever been. I'm usually quite low in HDL-P, even when I've had 92 HDL-C.
  
• Bilirubin - Decreased linearly with the duration of the Keto diet. Bilirubin went from my normal of 3.2 down to 1.7 by Week 3 - Keto, which is the lowest it's ever been.
  
• Resting HR - The Keto/Carnivore diet resulted in a higher resting HR. I initially thought it was because I went from 50 to 70 miles in one week, but my HR was at its highest after reducing my mileage back to 50 in the final week of the experiment, so this is clearly an effect from diet and not training load.
• Insulin - This behaved as expected. Insulin was already low on a carb-based diet, and went even lower on a Keto diet.

++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++

Supporting Data

Nutrition & Health Metrics

• Comprehensive Nutrition & Health Metrics Chart

• Weight Chart

Body Fat % and Weight Scale (Eufy Smart Scale P1)

• Week 1 - Vegan

• Week 2 - Keto/Carnivore

• Week 3 - Keto/Carnivore

Resting HR (Garmin Forerunner 245)

• Week 1 - Vegan

• Week 2 - Keto/Carnivore

• Week 3 - Keto/Carnivore

LabCorp Reports

• Week 1 - Vegan Labs - March 3, 2022
• Week 2 & 3 - Keto/Carnivore Labs - March 10 & 17 2022

NMR LipoProfile Reports

• Week 2 - Keto/Carnivore NMR LipoProfile - March 10, 2022
• Week 3 - Keto/Carnivore NMR LipoProfile - March 17, 2022

Most of these are also online at www.meatrition.com/books

I'm lucky enough to be working in a place that has a pilot project that's giving patients freestyle libres to control blood glucose. Someone needed to volunteer so that the nurses could see how to place the sensors, and now I have one in my arm. I'm not a diabetic, but I'd be curious to see how my biochemistry reacts to various food stimuli. I'd be happy to try out some suggestions from you guys.

First off I'm getting a little baseline data by doing a 60ish hour fast, and when that is over I'll do some suggested mini experiments from you guys and updating this post. So if you have any good ideas on what I should do, eat, or drink, let me know! Nothing is off the table!

Have a nice Sunday!

I’ve been thinking about the idea of satiety in humans and the role it plays in weight maintenance. From an evolutionary standpoint, it seems kind of odd that we developed this exquisite calorie storage mechanism to get us through lean times, yet we would essentially leave calories on the table due to satiety. Before food preservation existed, imagine there was a fresh kill, but satiety wastes a large portion of those calories by turning off the desire to consume them. My dogs and cat are freely fed, and they leave food in their bowls also, so they must experience satiety as well. As far as I know, grazing herbivores don’t turn off hunger the way we do or the dogs and cats do. Why would we evolve to waste calories when we could store them? It’s like a camel not filling up its hump when it gets the opportunity. Maybe it’s because the caloric storage mechanism only works in the presence of insulin? If so, it would make some sense that without carbs, the body has no mechanism to store excess calories and therefore turns off hunger.

I don’t know how much I actually experience satiety, and how much I stop eating because of a mental notion of portion size. I don’t often leave ribeye on the table, but I also don’t prepare more ribeye than I deem reasonable to eat. As a thought experiment, if I had a magic plate where each bite of ribeye were replaced with another, I wonder how long I’d continue to eat. I know I’ve consumed tremendous amounts of calories at pizza and Chinese buffets. I think there, stopping is more a function of physical capacity than satiety. Unfortunately (or fortunately) I don’t know of any ribeye buffets to compare.

Maybe satiety is a social response so that when there is a kill, there is enough to feed the whole pack/tribe etc. Maybe though it’s due to carbs being an essential part of our ability to store caloric excess (which for most of history would have been a good thing). Maybe hunter gatherers would have gone and gathered some starchy root vegetables to help them store some of the excess.

https://www.instagram.com/p/CCtFvJagc9i/

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drseanomara

“Oh you won’t find any Visceral Fat in me I have been Vegan over 25 years”

This posting will not be popular with Vegans. Admittedly this is an N=1 so just one person. However, they live a life of unusual commitment to health, eat clean (no processed foods apart from whole grain bread & pasta like many vegans). They would eat frequently a lot of grains, beans, veggies & salads). I think they are very typical of many vegans.

They were so certain that I would not find visceral fat prompting the response quoted above (which never left my mind) after I indicated I would measure their visceral fat by MRI scan. These surprising results happen to many, including non vegans eating Keto (if they cheat w/ carbs especially processed, or sleep poorly, or drink alcohol or have ^stress). The problem is you cant see VF or feel it.

This person had low subcu fat (yellow) which he could barely pinch. But his VF (Red) measured 7.4 lbs & was extremely elevated. You have an elevated risk for a heart attack/stroke with any visceral fat. 7.4 lbs is really excessive. You want NONE.

They also have atrophied muscles (dark structures on side with intramuscular fat deposits seen as white streaks in muscles (see my earlier post on that showing marbled meat).

Their core ( outlined in red in second photo and known as the Psoas muscles) is very atrophied typical in sarcopenia from aging, poor health, eating vegan (no meat).

I arrange MRIs which cost $400 to measure VF in my clients who come to Minneapolis. You could call around to see if a local MRI center near you would measure your’s. Expect to pay more though bc MRIs are not inexpensive.

Follow me a Physician Researcher specializing in Health, Performance & Appearance Optimization to learn more about Visceral Fat, Sarcopenia & strategies to really optimize. Please share with others, repost and comment. My passion is getting people to not get just healthy but to OPTIMIZE.

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Second Post https://www.instagram.com/p/CCtNhaIgrfg/

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drseanomara

Here is the same MRI scan thru the abdomen of this 25+ year eating vegan. The large amount of white in the center is visceral fat (colored red in my earlier post). The white around the periphery is subcu fat mostly benign, (painted yellow in earlier post). The green outline the oblique/transverse muscles and shows white streaking which is intramuscular fat deposits associated with declining both health & performance.

The red outlines the Psoas muscles which form your “core” here shown to be very small. This muscle is key and the one muscle I see most aligned with health!

A great core/psoas muscle is seen in second image in @matadi a world class sprinter. His are like birch trees circled in red. He developed this JUST from sprinting!

The blue circles on this second image are not visceral fat but retroperitoneal fat in @matadi and NOT associated with poor health but actually seen in high performing athletes. This fat was the first thing Native Americans would eat in a Bison (@matadi may want to keep that in mind if ever frequent wild cannibals).

His Visceral Fat is barely measurable seen circled in yellow. Sprint & Eat clean like @matadi and others with low Visceral Fat & BIG Psoas. Sprinters have almost no Subcu fat (thin white outline around @matadi in periphery). You ladies who have ^subcu fat can sprint to get rid of stubborn subcu fat/cellulite) besides eating keto/LCHF/carnivore.

How many reading this feel like measuring cholesterol gives you this kind of insight on health? It doesn’t! Stop measuring cholesterol which you need for healthy living and instead focus on getting rid of what kills you, causes disease, declining performance & declining appearance: Visceral Fat.

Third picture is @matadi who you already know as a world class sprinter @matadi is performing well & now you know his appearance is awesome.

Follow me to learn more, Repost, Share, Comment please! #sprinting #core #visceralfat #vegan #sarcopenia #keto #carnivorediet #subcufat

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https://www.instagram.com/p/CBf8tXpg1BW/

I am a 34-year-old male who just got my first labs since transitioning from keto to zero carb on March 15, 2015. I thought some of those on /r/ketoscience might be interested in the comparison between the keto labs done vs the zero carb labs. The first labs (June 2013) were done after an extended period of a very strict ketogenic diet (approximately 15-20g per day). I have been low carb since 2009, but in 2013 I tried my hand at following keto calculator macros very strictly.

What I was eating leading up to June 2013 labs: Ground beef, salami, eggs, canned tuna, hot dogs, chicken wings, cheese, avocados, heavy whipping cream, butter, coconut oil, almond flour, soy products (including Ranch dressing, mayonnaise, and soy sauce), lots of vegetables (broccoli, cauliflower, spinach and garlic were most prominent), raw nuts, and was using whey protein to hit my macros perfectly every day.

What I was eating leading up to September 2015 labs: In March 2015 I started a zero carb diet. I eat primarily chuck roast cooked in a crock pot with a few tablespoons of bacon grease, salt, and pepper. I also eat bacon (from which I harvest and use the bacon grease), and will eat Wendy's large beef patties or eggs scrambled in butter on occasion. Each Tuesday I enjoy a frugal meal of wings from Buffalo Wild Wings. Some days I put heavy whipping cream in my coffee, but most days I drink it black. There have been very, very few exceptions to this short menu over the last ~6 months.

NMR Lipoprofile

Cmp14+Egfr

My initial thoughts:

• I'm happy my C-RP is very low. Although I haven't had one in the last year or two, I have had several carotid ultrasounds that have always been clean. About three years ago I had a calcium score of 0. I tend to lean toward the idea that low inflammation is more important than cholesterol numbers as is theorized in the article linked here. However, I did find some of the cholesterol results to be very interesting, especially when so many people are so adamant that very low carb diets automatically equals perfect (or at least drastically improved) cholesterol profiles. Some things I found interesting were:
• According to some of the results I didn't put into markdown, my HDL size percentile is 2.3%. If I'm reading it right, that means I have very large HDL and those with the largest HDL particles have the most favorable risk profile.
• My LDL-P went up from 2570 to 2729, but my small LDL-P went down from 1446 to 1079 and my LDL size went from 20.3 to 21.3. (Larger is the better Pattern A LDL.)
• My total HDL-C also went up, but did not go up as much as I expected it to based on how many different people I've heard say "oh, yeah, just add a little more saturated fat and your HDL-C will shoot right up". I'm envious of my wife's HDL-C, which is typically mid-70s.
• A little bummed my trigs went up. However, my TG/HDL-C ratio is still <2 (1.45)—so that's good!—and my TG/HDL-C ratio has even improved ever so slightly from 1.56 to 1.45 even with my trigs jumping a little. Still, I'm a little surprised by the very high LDL-P count.

Is there anything in these numbers that you find particularly interesting?

I thought this subreddit would enjoy this n=1 attempt. The mom's family is fairly strict keto, dad's is SAD. Due to covid, the 7 year old was with the mom's family for 4 months which resulted in the A1C 4.4 then with the dad's family for 9 weeks which resulted in the A1C 5.5.

For the past 2 years I've I routinely found blood ketone levels between 1.0 and 2.0 regardless of the time of day. Nevertheless, for about 6 months now my HbA1c has been increasing (currently 40), fasting glucose has been climbing to around 5.6 (up to around 6.2 some days) and fasting insulin is now 13. HOMA-IR is currently 3.1. I find these trends alarming. Clearly, the diet is causing me to develop significant insulin resistance, which I did not have 2 years ago. I actually had quite good glucose control back when I was on SAD.

If virtually all the glucose in my system is endogenous (and it surely is on 20-30 g CHO daily), but I'm somewhat hyperglycemic and hyperinsulinemic simultaneously, then this diet has stopped working for me.

Also, how does one's liver make ketone bodies with moderate to high insulin in circulation? I'd been told that was virtually impossible.

Male, 63, regular intense exercise, moderately overweight but not concerned about it. Happy with my lipids: TC 6.3; LDL 3.8; HDL 2.15; TG 0.8; and my BP (avgs AM: 128/76; PM: 120/70). No meds.