It was a typically warm July southern Florida day as we pulled out of our hotel to find one exit blocked by construction. Google Maps sent us in another direction, and when that didn’t work out, we made our own map and, once again, hurried with time running out to our destination – the huge Veterans Administration (VA) building in Miami.
The big Miami VA was humming with activity.
The traffic, everywhere we went, was consistently heavy. Plus, Google seemed to have entered into a Bermuda triangle of its own, frequently telling us to go down one street and then do a U-turn. We made it to the building with minutes to spare. As we rushed through the warren that is the Miami VA – corridors everywhere – our confused faces must have given us away as we were helpfully directed several times to our destination.
I was there for a men’s ME/CFS exercise study. I was going to get on the bike, and exercise as hard as I could while getting blood drawn several times during and then after the exercise test. Dr. Klimas’s team was then going to analyze 9 million data points (covering gene expression, cytokines, flow cytometry, cell function, neuropeptides) captured from the test. This was all happening because of Dr. Klimas’s foresight in having chronic fatigue syndrome (ME/CFS) included as a control group for a Gulf War Illness study.
The idea of getting an exercise test and immune and other data was enticing and had prompted the idea of an East Coast trip, which ended up consisting of stops in Miami (Klimas exercise study), Baltimore (Vicky Whittemore and Avindra Nath interviews), Nashville (Dysautonomia Conference), Tuscaloosa (Dr. Skip Pridgen) and Birmingham (Dr. Jarred Younger).
So here we were in a small office in the big VA. Cognitive tests and the exercise test took up the first day and more cognitive tests were conducted on the second day. On the second day, I fasted in the morning, ate a prescribed breakfast at the facility, and then an hour or so later, did the exercise test.
Graham Salmun, the young exercise physiologist who provided the test, was very welcoming and more than happy to provide answers then and later in email. (It turned out that Graham, a triathlete, had had his own, thankfully temporary ME/CFS-like experience when he’d suffered from overtraining syndrome and was unable to exercise for a month.) It was testament to the strength of Dr. Klimas’s research program that by the time he got to me he’d done over 140 exercise tests in ME/CFS and/or GWS patients.
The test was explained, they got me on the bike, inserted shunts into both arms, and I started pedaling. I’ve done several exercise tests, but this one, for whatever reason, was the worst. It was a miserable slog all the way. I gritted my teeth and pushed as hard as I could until they stopped me.
Feeling somewhat loopy and sleepy after getting a saline IV, my partner and I went to the hotel, took a nap, and afterwards, for the most part, I was fine (!). That was the first time I’d gotten an IV after an exercise study and it worked.
The next day brought more cognitive tests and the scores from the first day’s tests, most of which were at or near normal range, but a few of which were not just low but shockingly low.
Graham, who has since moved on to a post-graduate program at another institution, was kind enough to go over some of the bike test results immediately.
Exercise Test Results
It turned out that I’d lasted for a long time on the bike – over 10 minutes, and could have lasted longer. That actually didn’t surprise me. About fifteen years earlier, ME/CFS and all, I’d actually outlasted my healthy twin, Cass, on the bike in an exercise study.
I regularly walk – not long distances – but I do it regularly enough that I assume I’m not deconditioned. The test did indicate, though, that I hit my anaerobic threshold early – in about half the time a healthy person would have.
Staci Stevens is able to mine an amazing amount of data from a cardiopulmonary exercise test (CPET).
Then Staci Stevens of Workwell – an exercise physiologist who has specialized in ME/CFS for years – took a closer look. Even after years of reporting on Workwell’s exercise results, I was astonished how much data she could get out of this report, which didn’t include several parameters (blood pressure, workload) that Workwell includes in its reports. (Those measures were taken but weren’t included in the data I was given.)
In general, my results suggested, as expected, that I have a mild to moderate case of ME/CFS. Even at that, it suggested I was probably not producing enough energy to comfortably carry on the daily tasks associated with living.
- Oxygen Uptake at VO2 Max – My oxygen uptake at max VO2 peaked at less than 75% of predicted. Since a sedentary healthy person would be expected to hit 85% of predicted, that result suggested to Staci that I had a metabolic issue that went beyond deconditioning.
- Oxygen Consumption at Anaerobic Threshold – My oxygen consumption at anaerobic threshold – 12.5 ml/kg – indicated a mild to moderate impairment. Since > 14 ml/kg provides the reserve needed to do daily tasks, I probably wasn’t generating enough energy to comfortably do the normal tasks associated with daily living.
- Heart Rate at Anaerobic Threshold – My resting heart rate was high (89 beats per minute (bpm)) and could have resulted from pre-test jitters. My heart rate at anaerobic threshold – the point at which most of my energy is being produced anaerobically – was a mere 98 bpm. That suggested, if the resting heart rate was correct, that I had a quite small activity window before my system spiraled into anaerobic energy production causing me fatigue and pain.
- Staci’s heart rate-based exercise program would have me keeping my heart rate below 98 bpm.
- Peak Heart Rate – My peak heart rate was 148 beats per minute, in the low normal range, but a good distance from 177 beats per minute (my expected maximum). That suggested that some chronotropic incompetence – an inability to get the heart rate up to speed – might be present.
- Ventilation and Breathing Frequency – my ability to move air in and out of my lungs – was very good – even better at 114% of predicted. That’s fairly unusual in someone with ME/CFS. But my breathing frequency (breaths per minute) at the end of the test was surprisingly low – just 30 breaths per minute compared to the expected 60. I was breathing more slowly, but possibly more deeply, as well. By the end of the test my body had been relying mostly on anaerobically produced energy for about 6 minutes. My lactic acid, which had built up enormously, should have been triggering my lungs to breathe more and more rapidly to buffer it. Staci suggested that the message to breathe more rapidly may not have gotten through.
- Stroke Volume – A graph showing heart rate and oxygen consumption suggested I may have lower than normal stroke volume. Stroke volume refers to the amount of blood the heart pumps out during each stroke. That suggested possible autonomic nervous system or cardiovascular issues.
- Effort – My respiratory exchange ratio (RER) indicated that I’d given a maximum effort.
Blood pressure or watts/workload measures were taken but not provided in the data I was given. The blood pressure results would have been interesting as blood pressure should increase during exercise, but in some ME/CFS patients, Staci said, it actually drops – a sign of autonomic instability.
Heart Rate Monitoring – Staci said that a heart rate 10 beats per minute higher or lower than usual upon awakening indicates that you’ve done too much. An early morning reduced heart rate, Staci said, is an ME/CFS thing – she doesn’t see it much otherwise, and it is also probably a sign of autonomic instability.
Biological Validation – The Univ. of Miami group I visited does not do biological validation to calibrate their machine – something Workwell recommends. Biological validation involves using a healthy person with known values to help calibrate the machine. My guess is that most exercise physiologists do not use biological validation, but in Staci’s experience, when biological validation is not used, the results tend to read higher (i.e. healthier) than actual. Therefore, my actual results might be lower.
A two-day exercise test done at Workwell or with Betsy Keller would have provided much more information on the resiliency of my aerobic energy production capabilities. I plan to do one at some point. Check out more on their two-day exercise tests below.
Exercise and Chronic Fatigue Syndrome (ME/CFS)
Salmun emphasized that he was providing his opinions based on his research and clinical experiences and that they may or may not comport with the experience of the others working with Dr. Klimas.
Salmun and Jeff Cournoyer, the lead physiologist in the study, recently presented an abstract on ME/CFS at the ACSM (American College of Sports Medicine) 2018 Annual Meeting and at the VA Research Fair. (Graham expects more studies from the exercise physiology arm of the study to come out.)
Salmun believes that some people who do fine on the test probably have autonomic nervous system problems. Otherwise, lots of different problems are showing up in the exercise tests, but one general energy production issue in both ME/CFS and GWS stood out: reduced metabolism of the key substrate in aerobic energy production – fat. In fact, Graham had just presented on this subject in Minneapolis at the 2018 ACSM conference.
That 20-person study (14 ME/CFS patients; 6 healthy controls) measured fat oxidation rates during a maximal exercise test in ME/CFS. The results were astonishing with maximal fat oxidation rates almost 50% lower in the people with ME/CFS (healthy controls – 617 g/day; ME/CFS patients – 339.5 g/day). While small, the study suggested that people with ME/CFS were indeed having trouble burning fats for energy while exercising – and provided another indication that people with ME/CFS are using anaerobically produced energy far more than healthy people.
To Graham Salmun, the problem likely seemed mitochondrial in nature. It’s in the mitochondria, after all, where fat/fatty acid oxidation is used to create ATP – our main source of energy.
Fatty acid oxidation
Salmun believes the energy deficits he’s seeing in ME/CFS probably result from two things:
- fatty acids aren’t being transported into the mitochondria properly; and
- they’re simply not available in the mitochondria to be utilized.
He referred to Booth’s study ‘Mitochondrial dysfunction and the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)‘ which found that the more mitochondrial dysfunction there was, the more severe a person’s ME/CFS symptoms were. That quite large (n=191) 2012 study, which Sarah Myhill co-authored, proposed that a major immediate cause of the mitochondrial dysfunction was a lack of “essential substrates” (as Salmun found).
Salmun noted that our bodies tightly control the oxidation of fuels in order to use the most efficient processes to produce energy. Breaking down muscles into amino acids, which are then converted into glucose using a process called ‘gluconeogenesis’, is terribly inefficient and is used only when absolutely necessary, such as during prolonged starvation states. Gluconeogenesis has been described as “an extremely expensive investment with a negative return”.
The concept of starvation has come up before in ME/CFS. In starvation and anorexia, amino acids and fats are used instead of glucose to preferentially feed the TCA or Krebs cycle and produce energy.
Chris Armstrong reported that many of the metabolomic anomalies (reduced amino acids and lipid and increased glucose) he found in ME/CFS are also found in starvation and sepsis. In these states proteins and lipids are used to maintain low energy levels while glucose is used for other matters – such as immune cell proliferation in sepsis.
Armstrong speculated that an infection or autoimmune process may have triggered a sepsis-like condition that resulted in a state of chronic cellular starvation.
Reduced “Autophagy”
Poorly functioning mitochondria do more than slow a cell and its functions down, though. If the mitochondria stay dysfunctional long enough, instead of entering a process of “autophagy” and safely recycling their contents, cells can become senescent, start deteriorating and begin secreting pro-inflammatory cytokines.
Salmun suspects that the broken mitochondria in ME/CFS patients’ cells, then, may be contributing both to the low energy in the disease and to systemic inflammation.
Dietary Help?
Intermittent Fasting
That autophagy issue gave Graham Salmun a clue on some possibly helpful dietary tips for people with ME/CFS. Studies on intermittent fasting/time-restricted feeding (IF/TRF) suggest that it can help cells with mitochondrial damage enter into autophagy and kill themselves off safely. Removing the cells with damaged mitochondria could provide a novel way of reducing inflammation and improve one’s ability to utilize fats for fuel and increase ATP production. Salmun thinks this dietary measure might provide a lot of benefit, in particular, to people with ME/CFS with high levels of mitochondrial dysfunction.
Time-restricted feeding or intermittent fasting involves restricting one’s food intake to a certain period of time – say from 12pm – 8pm each day. Outside of the 12pm – 8pm period, one should only drink water and not consume any calories, liquid or solid.
Check out Dr. Guido Kroemer, an expert on autophagy & intermittent fasting.
Courtney Craig, a nutritionist with ME/CFS, has found intermittent fasting to be very helpful.
High Fat, High Protein Breakfasts
If you eat more carbohydrates early in the day, your body will focus on carbohydrate utilization throughout the day. Graham recommended high-protein, high-fat diets, in general, for ME/CFS. Find out more about ketogenic diets for ME/CFS and FM below.
Exercise
Salmun’s prescription for “exercise” in ME/CFS was typical of exercise physiologists who know this disease: do short-term exercises (1 min or so) followed by a rest period of 1-2 minutes.
Conclusion
The results of the exercise test were personally illuminating (heart rate at anaerobic threshold = 98 bpm! Really???) but more exciting was the news that the Miami team appears to be finding problems with fatty acid oxidation – a core part of mitochondrial energy production. My attempts at intermittent fasting have not worked out but it’s clearly helpful for some people with ME/CFS and I will try again to get some more autophagy going and turn down the inflammation a bit.
Lastly, Staci Stevens’s interpretation of the exercise test results simply reinforced how much information these tests can provide. Workwell and allied exercise physiologists recently published a paper that reports on the unique responses people with ME/CFS have to two-day CPET tests and tells exercise physiologists how to do them correctly. A blog on that is coming up shortly.
Your Support Is Requested
Health Rising’s East coast trip provided a wealth of information inspiring the article you just read and the ones below. Next up on the agenda is a new treatment for fibromyalgia, an Avindra Nath interview, and – on the return home – the folks at the Bateman-Horne Center.
Travel provides many opportunities but travel to the East Coast, in particular, is expensive for a small organization like Health Rising which is still working on recouping its trip costs. If you find conference reports and other travel related blogs helpful and want to see these in the future, please support Health Rising.
Articles From the East Coast Trip
The Klimas’s Exercise Test
The Jarred Younger Series
- Widespread Neuroinflammation Found in Chronic Fatigue Syndrome (ME/CFS)
- Invasion – The Source of Neuroinflammation in Chronic Fatigue Syndrome (ME/CFS)
- Jarred Younger III : Treatments – A Better LDN and the Hunt for Microglia Inhibitors
The IVIG Series
- An IVIG Chronic Fatigue Syndrome (ME/CFS) / POTS Treatment Success Story: IVIG#1
- Are Chronic Fatigue Syndrome, POTS and Fibromyalgia Autoimmune Dysautonomias? IVIG #2
- The Case for IVIG Treatment in Chronic Fatigue Syndrome (ME/CFS), Fibromyalgia, Small Fiber Neuropathy, and POTS: IVIG#3
- Winning the Lottery: “Novel” Treatments Return Severely Ill POTS Patient to Near Health: IVIG #4
Advocacy
From the Dysautonomia Conference
- 2018 Dysautonomia International Conference I: Small Fiber Neuropathy, POTS, MCAS and Vagus Nerve Stimulation
- The 2018 Dysautonomia Conference Pt. II: Could You Have a Spinal Fluid Leak? An ME/CFS, POTS, FM Perspective
- Dysautonomia International Conference Pt III: The Autoimmunity Revolution in POTS
- “Sticky Blood” – Antiphospholipid Syndrome, POTS, Chronic Fatigue Syndrome and Fibromyalgia – The Dysautonomia Conference #4
- Stagnant Hypoxia – Where Chronic Fatigue Syndrome and Hyperadrenergic POTS Meet?
- Promise Fulfilled – A New Chronic Fatigue Syndrome / Fibromyalgia Practitioner Steps Forth
I still find it amazing that the entire CFS community was hostile to the first clue in the CFS syndrome.
Especially Cheney and Peterson.
And all “ME/CFS researchers” ever since.
But that was their choice, and hostile is what they continue to be.
https://www.healthrising.org/blog/2014/05/02/constant-vigilance-julie-rehmeyers-mecfs-recovery-story/
What is the first clue? And Why hostile to it?
Hi Cort – I continue to be fascinated at the different facets of ME/CFS. After having been on a ketogenic diet successfully for 2 years, with nearly pain being gone after the 6-month mark, my husband and I went on vacation. We decided that we would not worry about carbs and just eat what was put in front of us. By day 3, I had wrist pain, and by the end of the cruise, the pain encompassed both arms and shoulders and felt much as it had before beginning keto. As is my ‘normal’ recovery, it takes about 3X as long as whatever non-normal event to get back to whatever ‘normal’ is…so after 10 days, it would take about a month. And being at that point today, yes, the pain is now gone again (keto from the second we woke up the day after returning from our trip), but only just. I am hoping to get some relief from the cooler weather, but the holiday season kicks butt if I’m not careful!
On the other hand, I was having palpitations a couple of months ago, and since heart disease runs in my family quite seriously, I went through a host of testing, including a 30-day monitor and stress test. Didn’t even have to break into a run on the latter. I aced them all and came out with a less than 5% chance of an issue, so nothing to be concerned about. Have learned since then the palpitations were likely due to an electrolyte imbalance.
So interesting Lori and so good to hear it can take 6 months for the diet to take full effect. How quickly did you notice that it was having an effect? (I wonder if I didn’t stay on it long enough?
I was on keto for 3 months. It took me about 6 weeks to adjust and get back to a normal baseline because the body doesn’t know how to make energy out of fat. It takes a week to start making ketones but then 1-2 months to become fat adjusted and generate comparable and then greater levels of energy as when eating carbs. I too found it helped with aches and pains (and anger too interestingly).
@Cort: Did you quit your keto diet? Didn’t you report good early results or am I wrong?
@Chris: Anger totally makes sense: no need to push adrenaline to get blood glucose levels up with keto diet. You can get adrenaline up by both fear or anger. I far more often curse inside for near nothing since I’m ill, that’s just pushing adrenaline (in order to increase NADPH production) IMO.
Indirectly, I believe my (very) high adrenaline levels are part of why I have a really high pain tolerance: it increases NAPDH and IMO therefore reduces oxidative stress. The pain relief by going keto is probably due to reduced oxidative stress as well IMO.
But adrenaline can increase pain sensitivity just as well: it also increases “pain awareness” for better remembering dangerous situations. Maybe people getting more of an anxiety/fear effect from adrenaline are more likely to get increased pain levels with increased adrenaline levels?
Not by coincidence, 2 out of 3 FDA FM approved pain drugs are SNRI (indirectly increasing adrenaline) IMO. At least Cymbalta is. Works pretty well for reducing pain with me, but I’m lucky noticeable side effects and withdrawal problems are minimal with me. Still would like to have it’s benefit without the nastiness of high adrenaline ;-).
I was on it about a month. I think I had some mildly good results at first but nothing really significant. I didn’t have any significant negative effects.
I mostly follow a paleo diet now – still eating more protein and fat and fewer carbs. Protein bars in the middle of the day are my main transgression now.
The diet makes sense for me as eating things like potatoes and grains usually do leave me tired.
Heart function due to CFS’s viral infection can be improved. Low ejection levels (weak muscle) and cardiomyeopathy are common amongst people w/CFS (PCFS), since the virus goes from the brain to the Vagus and heart nerves.
Most CFS heart issues do not show up on Xrays, 1-day stress test (vs 2), or in an EKG.
Constantly low HRV of <40 (out of 0-100), is one sign of a vagus & heart nerve infection (Normal is 60-80, except the day after hard exercise). HRV can be checked each morning at home for ~$40 BlueTooth HR strap + EliteHRV or similar (free) app.
Paraphrased from health guru Anthony William (co-author of best sellers 'Life Changing Foods' & 'Liver Rescue'):
1. Try drinking an 8 to 16 oz glass of fresh celery juice every morning on an empty stomach, and see if the many special natural electrolyte salts in it help your heart function, brain function, and digestion.
Note: it may cause a mild detox reaction at first, so start with 4-6oz, or every other day.
Cost: Juicer+ $1/day
2. Take B-12 with the 'adenosylcobalamin' form of B-12 (1/2 dropper sublingually 2x/day) to help with any nerve issues.
'Vegansafe' B-12 on Amazon has that form included.
Adenosylcobalamin B-12 slowly helps with aches & nerve pain (incl. FM, MS), energy, and brain fog.
Per the late virologist Dr. Martin Lerner, MD (who had CFS himself & discovered the viral & ATP tie years ago):
3. For better ATP Energy production: Take as much magnesium per day as you can tolerate (add 'Calm' powder to drinking water is one easy way), and mostly in the evening (also helps relaxation).
4.CoQ10: 100mg 2x/day in the ubiquinol form (NOT the cheaper precursor UbiquiNONE <=take none!). Can cut down to once a day once feeling better.
5. D-Ribose, a special sugar, can help with cellular energy production and heart function (ejection strength). 5gm (1 big tsp.) 3x/day was typically used in the various heart studies, and up to 60gm/day was used. It can actually lower blood sugar, so be careful if diabetic.
…I use it in my lemon balm (anti-viral) tea. 🙂
6. Iodine/Iodide: It is a strong anti-viral.
12.5 mg/day (=same as tradional Japanese diet) is considered optimal'maintenance':
Iodoral tablets (1/day) or 2 drops Lugol's solution. Deficient people take 4x more; any excess is peed out.
Note: Iodide may cause 'detox reactions' if you are very toxic, so proceed carefully (see'Iodide' by Dr.David Brownstein,MD)
7. Selenium +200mcg/day, & max. of 400mcg (avg) from all sources. (Dr.J.Wallach,ND). Helps heart, thyroid, cells.
8. Zinc. We are all low. Take extra zinc lozenge or two daily. Helps energy & immune system. Also clears up skin.
Anti-Viral Diet advice from Anthony William (see his 4 books for the details):
Rule #1: Do not feed and support the HHV viruses.
Cut out the mucus-producing & inflammatory foods such as gluten, ALL dairy (incl. butter, yogurt, cheese), unfermented GMO soy (tofu), and eggs (=what vaccine mfrs use to quickly grow viruses!).
Avoid pork fat and all processed vegetable oils. Avoid Canola Oil, MSG ("natural favors"), citric acid, and all frankenfoods with a long shelf life.
Eat a low fat 'clean' diet high in organic veggies and fresh or frozen fruits and berries.
All fresh fruits & berries are considered anti-virals and anti-oxidants; whatever natural sugars are in them help drive their nutrients into your cells. It is best to have a little fruit (i.e half an apple, a few slices of Avocado, a handful of berries) every 1.5 to 2 hours, so as to stabilize blood sugars and adrenal glands. After adapting to it, you should then never be hungry.
A low carb/high fat diet stops working after about 4 months and clogs the liver. …If you are no longer easily losing excess weight on it, have the start of insulin resistance (fasting blood sugar over 100) or diabetes, no extra energy, blood triglycerides over 100, and/or survive mostly on coffee (i.e. adrenaline), it is time to refine it.
"Intermittent fasting" works by giving your overworked (and EBV viral-infected liver) a break. The liver filters the blood and sends 'fresh' & nutrient-filled blood directly to the heart. When you then eat foods with ANY fats (i.e all meats, nuts, etc.), the Liver switches to mostly bile production and food processing.
More filtering, 'defatting', and healing the liver can be done by limiting eating fats and proteins (thus most your calories & all your hard to digest foods) between noon and 8pm. It gives the (fatty) liver more time to simply filter and heal ('rest & digest').
Upon waking, have 1/2 lemon in 16oz water first thing, then celery juice 20 min. later; then melon, raw or steamed veggies, fruits, and/or a big 'green shake', but ZERO fats, ZERO meat protein, and ZERO processed sugars (besides D-Ribose). Have protein only at lunch & dinner. Fill up on veggies, quinoa or rice, and some lean meat (if Paleo) or some nuts and seeds (if vegan).
Switch up step by step as you find suitable replacements for favorite foods at Costco, Trader Joes, Amazon.com, Whole Foods, and your local supermarket, and ways to adjust favorite recipes.
The above has successfully been used by thousands with CFS, FM, MS, RA Lupus for 35+ years. I assume most readers here are familiar with the above two authors and are already doing some of their healing protocols.
My FM pain suddenly disappeared one day last year, and I can now bicycle 12mph on flat roads to Starbucks 2x/wk with a bunch of other retirees.
My 'Nutritarian' adult son's daily migraines are now a lot better from all the celery juice and B-12, too.
Try upgrading your diet for a month (after easing into it over a month or so) and see if it helps you!
Any carb seems to make me more hungry. I thought I was being really good by having vegetable soup yesterday but it made me feel really hungry.
Many of these seem like excellent ideas to me. Thanks for putting them together out ex-athlete. I do notice that COQ10 (Costco) is helpful.
Could be also the holiday was a physically and mentally stressful event that triggered PEM and not carbs. Not saying that for sure but it’s possible
Question:
In going off your low carb ‘keto’ diet while on vacation, how much of the added carbs was gluten (breads and pastries), processed sugars, beer, GMO soy/tofu, and milk-dairy (ice cream, butter, lattes)?
Did you also have more energy while off the keto plan? It seems like you did a lot on your trip, unlike a lot of CFS people.
As for the relapse:
It may be the mucus-causing & virus-feeding foods, not the fats vs carbs, that caused the old issues to flair up again so quickly.
It seems like the keto diet was just suppressing the EBV symptoms, vs rebuilding the immune system & making you healthier.
Usually it is a physical, chemical, or emotional stress (like a death, or divorce) is what triggers a relapse; Not a fun vacation or a yummy danish!
Note that a continuous high-fat diet is really hard on the EBV-infected liver in CFS people. It eventually clogs the ‘fatty’ liver, sending the resident virus and toxins elsewhere.
…Thus creating the 94 EBV-related chronic diseases and cancers found in the April 2018 Cincinnati Children’s Hospital EBV study.
What to do in the future?
Remember all fresh organic fruits and berries and many herbs are anti-viral and/or anti oxidants. The various natural sugar complexes in them are what drives the nutrients into our cells (it is how we evolved).
These phytonutrients, enzymes, and anti-oxidants are important when trying to rebuild the immune system & recover from ME/CFS, F.M, or any other viral based illness.
So after the first 2 weeks of very low carb, add back fruits & berries. Their ‘viti-sugars’ are NOT the ‘bad’ (empty) refined sugars we should all avoid. Just have the melons, fruits, and/or berries in the morning and for snacks during the day, when their sugars & nutrients will be ‘driven in’ & used up immediately.
Ketosis should just occur during the later stages of sleep, or in extended exercise (think tracking an injured prey animal, or marathons), as it was designed to do.
Dr. Mercola recommends cycling diet plans every few days and/or months, since the body will adapt to ANY diet via compromise.
We do not want our body storing extra (toxin-filled?) fat nor compromising the immune and cancer-fighting systems. Maximizing the liver’s filtering capabilities is our best bet.
So taking a break from keto, Paleo, Vegan, Atkins, Virgin, Gershwin, Hawaiian, Blue Zone, Slimfast, or whatever the latest diet fad is, can be good. Each has its good and bad, and all include learning how your body reacts to various foods. Keep a food log that also notes hunger levels, timing, and mood.
Whichever Diet includes the most fresh organic foods and nutrition (including phytonutrients and enzymes) and the least amount of arsenic, DDT, heavy copper, mercury, and other toxins is best. It varies region to region and season to season.
If you don’t want to think about your health & diet that much while traveling on vacation, in some parts of the world (Italian countryside? Costa Rica?) they still have ‘heritage’ (organic non-GMO) wheat, soy, corn, etc. to feed you AND the livestock, so maybe plan your next vacation there, and stay in a family-run Inn with locally sourced food.
Search for the most delicious fruit, not pastry or cheesecake!
And drink wine or filtered water, not beer (<=gluten).
Hi Cort,
Thanks for traveling around the States, doing tests and interviews and reporting them to us! You’re the best ;-).
“after the exercise. Dr. Klimas’ team was then going to analyze the 9 million data points”
Now that is a whopping high number! Imagine doing that by hand in the 60’s!
“That 20-person study… …The results were astonishing with maximal fat oxidation rates almost 50% lower in the people with ME/CFS (healthy controls – 617 g/day; ME/CFS patients 339.5 g/day).”
Now that is some data! It probably tells that in a ketogenic diet it’s not burning the fat that does the magic, and that going for a non-ketogenic fat-heavy diet might be questionable for ME patients.
Going with the whole NADPH thing being anti-oxidative stress, I am not surprised fat consumption (for non keto) ME patients is low. It’s a wasted opportunity to produce NADPH from that point of view.
If we look at the quoted 20-person test, then I am really interested to know if they kept track of the fat oxidation rate before and after exercise. If the NADPH idea held value then I would not be surprised that the fat oxidation rate remained reduced compared to the rate before exercise and that the fat oxidation curve over the day looked different compared to that of the healthy controls.
The idea here is that ME patients would be left in a high ROS low glutathione state for many hours (about one hour) after the test, shifting to low NADH and high NADPH production going hand in hand with turning down fat consumption and increasing glucose consumption for the PPP (and feeling depleted from being barely able to produce ATP).
The one hour margin is for leaving time for the anaerobic oxygen debt to be cleared out. IRC, it also goes with the about one hour delay until ROS goes very high after exercise thing you mentioned recently. Wasn’t that also a Klimas study?
I don’t know how sensitive such measurements can be done, but if a ME exercise test were done in the (late) afternoon, I’d be not surprised (in line of the NADPH idea) to see nightly cholesterol (and trygliceride) production to be down too. Would anyone have done such test with ME patients ever?
I’ve seen incredible improvements since starting the ketogenic diet and have been IF (20/4) for over a year as well. I’ve always failed to understand why these have helped me so much but I am grateful, even though I’m still not 100%.
Glad to hear and thanks for passing that on Kyle. For people interested in a ketogenic diet you can find more resources in Health Rising’s diet section – https://www.healthrising.org/forums/resources/categories/diet.172/
I take NT factor for lipid replacement therapy and although it makes me tired for an hour or so the long term benefits are astonishing. If I take the dose every day within a month my activity levels increase steadily. NT factor works by replacing the inflamed membranes of mitochondria with newer healthy lipids. That why it take so long. I take the allergy research brand powder.
But my breathing frequency (breaths per minute) at the end of the test was surprisingly low – just 30 breaths per minute compared to the expected 60.
With regard to what you wrote, I thought I would let you know I was exactly the same on the test on my Autonomic Function at the Breakspear about 5 years ago. I just seemed to breathe very slowly but deeply, about half that of a healthy person. (I used to think that was a good thing having done yoga and pilates on and off for over 40 years).
Also like you I am able to walk most days but never for longer than 25 minutes but if suffering with PEM then only 10 minutes exercise will wear me out. Thank you Cort for giving us all this fascinating information which I hope will soon result in a treatment to improve this basic problem of not being able to regenerate energy like a healthy person.
“But my breathing frequency (breaths per minute) at the end of the test was surprisingly low”
Is that for cycling only? To me, (very low intensity) cycling allows me to breath *really* slow, sometimes a lot slower then at rest. Other sports/activities don’t.
I don’t know. It was at the end of the test. I had assumed that it simply something that would show up during any exhausting exercise but don’t know.
How interesting! I would have thought the same but I guess when at the point of exhaustion when lactate is building up – it’s best to breath really fast – otherwise the lactate doesn’t get buffered and continues to build up. I wondered if my high levels of ventilation were compensating for that a bit (???)
” I would have thought the same but I guess wen at the point of exhaustion when lactate is building up – it’s best to breath really fast – otherwise the lactate doesn’t get buffered and continues to build up.”
It does make kinda sense to me. It probably means your body does not want to prevent lactate buildup. Let us assume that the main goal of the body is to prevent exercising too much. Then:
* If your body would do plenty of breathing effort to reduce lactate buildup then you would just continue to exercise longer and end up with just as much lactate in the end when you can’t keep it up anymore. That would give you: just the same amount of lactate 5 minutes later, 5 minutes more of damaging exercise and 15 minutes of more exhaustion of the “breathing muscles” compared to only 10 minutes (if that was how long you lasted now) of more moderate “breathing muscles” exhaustion now.
=> So if you breathed more in order to reduce lactate you wouldn’t get lower lactate at the end and exhaust yourself way deeper.
=> As your breathing would be a lot more exhausted, you would be unable to breath well enough long time afterwards to “repay” the oxygen debt after anaerobic exercise. That would in fact cause a prolonged delayed upshoot of lactate buildup over the hour(s) after the exercise. So lactate buildup would be even worse by trying to breath deeper in order to get rid of it during the exercise.
=> As for the massive production of ROS, once it would overwhelm the anti-oxidant defenses then it starts to “take over” the RBC impeding breathing and oxygenation severely for a long time. It acts a lot like a half carbon monoxide poisoning. I believe breething deep and slow is a pretty good breathing technique to expell it. Breathing faster can up the rate a bit, but it’s more important to keep it up long time as ROS (according to what you mentioned recently) is elevated in a delayed but long lasting way. “Breaking” your breathing ability during exercising would be a poor choise here.
=> So Breathing deep and slow-ish during (and for a long time after) the exercise seems to be the better choise for a person with ME and that’s what you did. Breathing deep and fast is kinda PEM doubler IMO.
Note also: going high (and prolongued) lactate helps to shut down the anaerobic glucose to pyruvate/lactate pathway and therefore allows to channel more of it in the NADPH producing PPP.
Cort, as I was reading your results, I was surprised that I seem to be similar, even though I haven’t had the extensive testing like you. You are also blessed with that great brain and so even if it might show some slight issues, compared to others, it surely is functioning way above par!
Currently I am participating in Dr. Klimas MTHRF double blind study and I have found her associates, like you described, very forthcoming and helpful.
Regarding the keto diet, my partner who has been doing it for over 6 months (mostly for weight issues), has had problems with cravings. Personally, I think when a diet is so restricted (as how he is practicing it), that the body, in its innate wisdom, will signal the brain to supplement missing nutrients. (And by this I don’t mean refined sugars and starches which are rather an addiction than a nutrient).
These intense cravings (and subsequent cheating) are sabotaging his effective weight loss. He eats too much of ketogenic foods, also sabotaging the slightly restrictive caloric ideals of this diet.
I don’t know what the answer to this problem is (special diets or what?), especially since everybody is different. For myself, learning how to carefully listen and track how my body feels after what it eats (or doesn’t eat), has been most helpful. I also ‘listen’ to any cravings as they are messages as well. Time consuming I know, but a much better fit in the end.
Glad to hear you are in the MTHFR study Nancy.
I certainly salute your partner’s commitment and I think, like you, that after all this time his body is probably telling him something. The keto diet doesn’t work for everyone. Diet seems like such a heterogeneous thing. I wonder if a modified Keto diet would work better?
Hi Cort,
So glad you were able to make it down to Miami and participate in the study. While I can’t say the Keto diet has helped my CFS symptoms, I can say that it has helped my mood immensely, which makes everything a lot more bearable :). While you were down there did anyone on the Klimas team mention anything about the start date for the CFS trials in post-menopausal women, and men? The last video she posted back in October on Nova’s website she said that the GWI had begun and has had positive results so far (n=1), and that the CFS trials should be starting soon.
I last spoke to Dr. Klimas in September. At that time she said the post-menopausal ME/CFS trial would begin this fall. I haven’t heard anything since then. I will try and find out.
I got the impression from Breakspear that they thought I was just breathing incorrectly and that with some guidance I could correct this! I am positive they mentioned some form of special exercise I could do to achieve this but to be honest it never made sense to me so I didn’t bother.
During the test at Breakspear on my Autonomic Nervous System Dr M said that I had severe cellular hypoxia because at one time I had only 50% of oxygen in my cells compared with a healthy person and at times I had slightly too high carbon dioxide instead. She told me this was very bad for me and I would benefit from using an oxygen concentrator 5 L/min for up to an hour and 3 times daily. So I have been doing this for about 5 years now I do feel better after a top-up but now only use it for 30 minutes max at a time.
I do wear a Fitbit Alta HR wristband and can see my resting pulse when asleep is between 56-62 but when I go for my short walks at a normal pace for me which isn’t particularly slow my hr is usually between 108 – 120 which is probably too much for a 70 year old. However I have found no correlation between the lower number or the upper with regard to how I feel after. In fact when in PEM and I go for a shorter 10 minute walk I will often see HR is 108 and yet at the end I am worn out more than when its 120.
Probably should add that I do take a very low dose of Propananol 10 mg before getting up in the mornings and sometimes later in the afternoon because of a tendency towards POTS.
I got into remission from cfs with high fat low carb diet with copious amounts of ALA and lots of glutamine. Peripheral neuropathy and POTS disappeared.
Aerobic ability increased dramatically and HR stays lower during exercise.
I tried it before without success but I didn’t have enough fats. Olives are my staple.
Any questions just ask.
Had cfs for 5 years. Was moderate.
Nice! Thanks for providing that.
On a scale of 1-10 with ten being perfectly healthy how are you now?
Hi cort
Hover from 8 to 9.
I can dip to 5 real quick if I cheat on diet etc but rebound to baseline real quick.
Was housebound at worst about 3 years ago.
When your adrenal hormones are shot it makes CFS X10 worse.
Adrenal symptoms I was getting are totally resolved….erratic racing heart…..erratic adrenal surges….poor blood sugar control…feeling of impending doom….libido loss….etc etc. POTS was last to go and it can still flare. It seems a real stayer.
You have my email cort…fire me over anything u need.
I was a active member on PR for 6 years.
Regards
Somewhat off-topic but it was lovely to see your researcher using the work of Myhill, Booth et al. Norman Booth was a member of our local ME group because his wife has ME. Sadly, he died a few months ago.
I have always felt that their wonderful research was under-utilised because it was independently produced (even though Norman Booth was an Emeritus Professor of Physics at Masefield College, Oxford). I’m so pleased to see that it was quoted here.
Couldn’t agree more Diane.
Poor ATP recycling they discovered years ago but I think still lack of root cause from the study left it in the wind a little.
Hi Diane, Greg,
Is this research about poor ATP recycling? If so, could you PLEASE provide a link?
Poor ATP recycling could be the direct cascade-consequence of too high NADPH depletion especially during PEM.
The idea in short is, with supposed plenty of semi-permanent high oxidative stress glutathion is in very high demand, putting very high demand on NADPH and its recycling. If NADPH gets too low then NADH and ATP production must be reduced. During exhaustion glutathion and NADPH status tanks and consequentially the body must sink NADH to very low levels too. That leads to necessary destruction of NAD+/NADH.
When the exertion/exhaustion/PEM is over NAD+/NADH/NADP+/NADPH levels needs to be restored.
Several pathway for reconstructing NAD+/NADH/NADP+/NADPH from scratch seem to consume (like in permanently remove) ATP:
Pathway 1:
https://en.wikipedia.org/wiki/Nicotinamide_adenine_dinucleotide: NAD De Novo construction:
“Most organisms synthesize NAD+ from simple components… …by transfer of a phosphoribose moiety.”
=> Now NAD+/NADH contains several phosphor groups and it must come from somewhere. Looking further into this unknown “phosphoribose moiety” I did found https://www.britannica.com/science/metabolism/Anaplerotic-routes#ref507806 “accepts a pentose phosphate moiety (reaction [73]) from 5-phosphoribose 1-pyrophosphate (PRPP); PRPP, which is formed from ribose 5-phosphate and ATP”
=> RECONSTRUCTING NAD+/NADH AFTER (SUPPOSED) DESTRUCTION BY PEM DOES DESTROY ATP!!!
One more ATP consumer/remover I did found was “In a further step, some NAD+ is converted into NADP+ by NAD+ kinase, which phosphorylates NAD+.[23] In most organisms, this enzyme uses ATP as the source of the phosphate group” in https://en.wikipedia.org/wiki/Nicotinamide_adenine_dinucleotide
https://en.wikipedia.org/wiki/Nicotinamide_adenine_dinucleotide
“The effects of the NAD+/NADH ratio are complex, controlling the activity of several key enzymes, including glyceraldehyde 3-phosphate dehydrogenase and pyruvate dehydrogenase.”
Now controlling pyruvate dehydrogenase has a clear effect on energy production in our disease. But there is far more.
I looked into https://en.wikipedia.org/wiki/Glyceraldehyde_3-phosphate_dehydrogenase, something also controlled by the NAD+/NADH ratio, which is affected by the NADP+/NADPH ratio as the ratio between NADPH and NADH must be maintained between relatively tight limits as well.
“GAPDH has recently been implicated in several non-metabolic processes, including transcription activation, initiation of apoptosis,[5] ER to Golgi vesicle shuttling, and fast axonal, or axoplasmic transport.”
and it interacts with plenty of components (see Protein binding partners section) but it interacts also with (see Nucleic acid binding partners section):
“GAPDH binds to single-stranded RNA [30]and DNA and a number of nucleic acid binding partners have been identified:”
and there it show a list of RNA and four nasty viruses (and maybe more to be found?)
=> NADPH status effects GAPDH by modifying the NAD+/NADH ratio and this GAPDH can bind to a number of nasty viral DNA. The importance of this is unknown, but may be significant in a disease often triggered by viral hit and run.
Also in https://en.wikipedia.org/wiki/Glyceraldehyde_3-phosphate_dehydrogenase
“Metabolic switch
GAPDH acts as a reversible metabolic switch under oxidative stress.[13] When cells are exposed to oxidants, they need excessive amounts of the antioxidant cofactor NADPH. In the cytosol, NADPH is reduced from NADP+ by several enzymes, three of them catalyze the first steps of the Pentose phosphate pathway. Oxidant-treatments cause an inactivation of GAPDH. This inactivation re-routes temporally the metabolic flux from glycolysis to the Pentose Phosphate Pathway, allowing the cell to generate more NADPH.”
Now this one gets interesting:
https://en.wikipedia.org/wiki/Nicotinamide_adenine_dinucleotide_phosphate
“However, there are several other lesser-known mechanisms of generating NADPH, all of which depend on the presence of mitochondria. The key enzymes in these processes are: NADP-linked malic enzyme, NADP-linked isocitrate dehydrogenase, NADP-linked glutamate dehydrogenase and nicotinamide nucleotide transhydrogenase.”
I was searching for a more exact way of how the Krebbs cycle could turn from producing NADH to producing more NADPH. It was needed to understand how people on a keto diet recycle glutathion. Seems it is wright here.
According to https://en.wikipedia.org/wiki/Isocitrate_dehydrogenase there are 3 isoforms of Isocitrate dehydrogenase (IDH): IDH1, IDH2 and IDH3.
Only IDH3 is producing NADH “In humans, IDH exists in three isoforms: IDH3 catalyzes the third step of the citric acid cycle while converting NAD+ to NADH in the mitochondria.”
“The isoforms IDH1 and IDH2 catalyze the same reaction outside the context of the citric acid cycle and use NADP+ as a cofactor instead of NAD+. They localize to the cytosol as well as the mitochondrion and peroxisome.”
That means IMO that IDH1 and IDH2 can perform the “This is a two-step process, which involves oxidation of isocitrate (a secondary alcohol) to oxalosuccinate (a ketone), followed by the decarboxylation of the carboxyl group beta to the ketone, forming alpha-ketoglutarate.” process both in and outside (in the peroxisome) the mitochondria.
=> IMO IDH1, 2 and 3 can continue the conversion of isocitrate to oxalosuccinate to alpha-ketoglutarate.
=> IDH3 is a classic “Krebbs” process, needing isocitrate plus NAD+ as an input and producing alpha-ketoregulate plus NADH as an output, only in mitochondria
=> IDH1 and IDH2 are unclassic, needing isocitrate plus NADP+ as an input and producing alpha-ketoregulate plus NADPH as an output, in mitochondria and peroxisome
=> This is one clear way of how to turn (part of) the Krebbs cycle away from NADH to NADPH production to supplement NADPH production through the PPP.
=> NADPH production through this way may well be an essential thing to “advance” the cycle by converting isocitrate to alpha-ketoregulate if this was a rate limiting step in the Krebbs cycle (and thus ATP production)
Note https://en.wikipedia.org/wiki/Nicotinamide_adenine_dinucleotide_phosphate “The isocitrate dehydrogenase mechanism appears to be the major source of NADPH in fat and possibly also liver cells.”
=> Is this why the “brown fat” (people that sleep in colder rooms have more of it) research pointed out by Cort I think in the sleep section says it reduces oxidative stress or something like that?
Side note: “The reaction is stimulated by the simple mechanisms of substrate availability (isocitrate, NAD+ or NADP+, Mg2+ / Mn2+ )”
=> high success magnesium supplementation in many ME patients?
glutamate dehydrogenase activity is also an interesting one.
“NAD+(or NADP+) is a cofactor for the glutamate dehydrogenase reaction, producing α-ketoglutarate and ammonium as a byproduct.”
“glutamate dehydrogenase activity is raised in order to increase the amount of α-ketoglutarate produced, which can be used to provide energy by being used in the citric acid cycle to ultimately produce ATP. ”
=> It can convert (some) amino acids to feed part of it through the Krebbs cycle. In doing so, by “selecting” the wright mix of isoforms it can generate either NADH (2 isoforms) or NADPH (1 isoform). All do generate NH3 (ammonium). If this ammonium gets succesfully converted in uric acid then it generates a non recyclable anti-oxidant with the same strength as vitamine C / asorbic acid. In theory Vitamine C is much more potent as it can be recycled but this recycling requires NADPH so when NADPH is really short it lijkely is a one way use (strongly reducing anti-oxidative working of vitamine C). If the body puts emphasis to the NADPH producing isoform and is able to produce uric acid out of the waste then it has produced a double anti-oxidative effect per conversion of a single amino acid.
I start to believe that the (supposed by me) very fast consumption of amino acid during exhaustion may be the thing delaying the high amounts of ROS by about an hour as reported in recent research if I recall well what Cort wrote in a comment. The conversion of ammonium to uric acid may temporarily take over the role of glutathion when its depleted. When both are depleted we get to the next stage of PEM.
Now https://en.wikipedia.org/wiki/Malic_enzyme is another interesting one.
Now there are 2 isoform producing NADH from (S)-malate and 1 isoform producing NADPH from (S)-malate
There is one enzyme producing NADH from (R)-malate
The interesting thin here is that all of the reactions are of the form of
(S)-malate + NAD+ ⇌ pyruvate + CO2 + NADH
(S)-malate + NADP+ ⇌ pyruvate + CO2 + NADPH
(R)-malate + NAD+ ⇌ pyruvate + CO2 + NADH
=> They produce PYRUVATE, early leaving the Krebbs cycle!!! See https://en.wikipedia.org/wiki/Citric_acid_cycle#/media/File:Citric_acid_cycle_with_aconitate_2.svg
=> They do something that seems very wastefull by not producing NADH plus oxaloacetate and continuing the Krebbs cycle
=> Instead they produce pyruvate, something that is already very high in ME patients. This pyruvate could be easily lost to the Krebbs cycle. However research has shown that higher pyruvate levels protect the brain from oxidative stress. It also alligns with my believe that the body wants to increase pyruvate in order to shut down glycolysis in order to shift more to the PPP and it offers a simple and straightforward way to produce glucose for people on a keto diet (by converting pyruvate in the liver to glucose). It also allows to reduce the amount of NADH produced by the Krebbs cycle, then to convert the pyruvate to glucose in the liver and then to feed the glucose to the PPP allowing a strong shift away from producing NADH to NADPH (and less ATP/energy)
Greg, I feel that the metabolic trap hypothesis could well prove to be the root cause. That one excites me.
For years people have been saying ‘This is the cause’ and I’ve been thinking ‘No, that’s a symptom.’ Once you start looking at gene variants, you must be getting to a cause. I have not read up on the kynurenine pathway, and it will have to wait for another month, but it does seem to connect elegantly with things like ATP.
Dejurgen, good luck with all your thinking and research.
I think you’re right.
I initially missed the significance of Booth’s work but it’s turning out to out to be quite prescient isn’t it? He was another in a long list of pioneers who have supported people with ME/CFS.
Dejurgen, here are links to their three papers.
http://www.ijcem.com/files/IJCEM812001.pdf
http://www.ijcem.com/files/IJCEM1204005.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3515971/
It was an interesting partnership. Dr Myhill has been treating ME patients here in the UK for years. Dr Booth had a background in physics and after he retired, and his wife became ill with ME, he transferred his research skills to ME. He collaborated with Dr Myhill, offering to write up her work. John McLaren-Howard is also retired but developed tests specifically for ATP functioning, etc. So here we have a group of three very intelligent and committed people, working together in their own time with no financial backing and producing astounding results.
Norman attended every conference he could and spoke to as many researchers as he could. It is because of his dedication that we now have Dr Karl Morten working on the problem here in Oxford. Norman interested Karl in the work.
Thanks a lot Diane!!!
I did read it diagonally. I’ll do a further in dept reading later.
I posted some more work I did yesterday concerning the link between ATP recycling/NADPH recycling/glutathion. It’s unstructured but that’s the best effort I can afford for now. I’m surprised WP let me spam the forum that much already; it blocks me for less. Sorry Cort ;-).
Together with much I wrote on previous blogs about my views on the importance of NADPH recycling and a slew of other ideas that would further decrease readability it forms IMO:
* The description of one giant energy blocking mechanism that is deliberately enforced by the body in order to stave of truly exceptional amounts of enduring body wide oxidative stress.
* The whole NADPH/glutathion/ATP deficiency seem to be together with a significant number of identified controlling enzymes all related and working in concert to achieve the above goal.
* It seems to be in line with recent metabolic research including the reported levels of pyruvate, lactate, certain amino acids, phosphor components and apparent dysfunction of key processes like glycolysis such as is seen in Naviaux’s and other researches.
* So far, the combination of these ideas plus some other unmentioned ideas strongly seem to lead to a coherent framework that, once one assumes that there is a strong ongoing trigger of huge oxidative stress generation, can explain the bulk of all energy related issues in ME in a manner in line with current medical science.
=> This may unify the previous work of Myhill, Booth et al., Rich Van K and my early NADPH recycling hypothesis into something far bigger then the sum of its components.
I very rarely make such bold statements, but I believe we may be looking at the generic energy blocking mechanism in ME and be able to describe large chunks of it in term of standard medical science.
This is the very first time I feel some of my ideas are robust enough to move to the next stage of validation or renouncing. I’ll have to let it sink in. When I still feel the same way about this in a few weeks then I could really use help in improving ordering and structuring of these ideas, remove inconsistencies, fact checking, request people submitting counterarguments/facts…
As to what the source of this massive enduring oxidative stress is, that is probably vastly more divers then this seemingly (near?) universal energy blocking mechanism. I’m working on a similar model that is in line with recent science for mine.
As usual, fascinating and informative stuff. Thanks Cort.
Sorry, I can’t read all the comments, so don’t know if this has been covered already.
Why, when it’s been shown that folks with ME/CFS don’t metabolise fats well, are we recommended to go on a KETO or Paleo diet that is high in fats?
I don’t understand, how come it works for so many people?
I’m not sure but I think it may force the body to focus more on fats – the best energy resource – and back off from its focus on carbs (?)
No way can i go keto, i can manage fat well, or too much protein i do slightly better on good carbs but struggle with all foods. Im severely affected totally homebound 8 years.
The idea of fasting i tried can’t do that either but i naturally don’t eat for about 16hrs as i can’t eat late at night and i don’t get up to eat early, so i go through the night of about 16hrs with no food which ironically is the 16:8 suggested fasting diet. Yet its done nothing for me so this idea of autophagy through fasting obviously hasn’t worked for me.
I eat vegan for the animals but i haven’t seen much improvement in my health. I can’t eat raw, i can’t eat sugar even fruits are limited and i have to be careful with fat and protein and carbs but out of the 3 i say good carbs are easier for me than fats and proteins, but severely affected and still unable to sit upright for long or chat for long and totally homebound 8 years shows something is seriously not working and diet isn’t the answer for me.
I’ve supplemented as well and i eat clean. I wasn’t vegan when i got ill so that didn’t contribute to my ME. I was very fit played several sports, good life, got a virus never recovered. Of good mental health even being in my situation i am string mentally among the severe brain fog. Its a mystery this illness to me, and i don’t find anything is helping, so its acceptance, compassion and kindness and see what happens.