I was keen to understand why all the low-carb diet resources tell you to eat more salt. I therefore decided to look into this in greater detail. The problem I encountered was that nothing actually states the reasoning behind it; sources merely allude to the requirements, then make recommendations on how to achieve them.
What I was keen to understand in particular, is the role of insulin in causing the kidneys to retain salt. The below is what I’ve managed to piece together.
As always, I must state that I have no medical or dietary training; all I can do is try and present the results of my own reading in as clear and jargon-free way as possible. If readers’ comments can help guide my understanding, then all feedback will be gratefully received!
So here goes… Salt!
When you switch over to a ketogenic diet, you’re effectively changing the way your body creates and burns energy.
On a glucose-based metabolism, the energy-form ‘glycogen’ is produced in the liver. This energy is water-soluble and transported around the body in your blood. The blood-stream is therefore our ‘road-network’ for distributing energy to all the cells and muscles that need it. Glycogen is also stored in the muscles, so the blood-motorway serves to ‘top up’ these stores when required.
Because glycogen is transported in liquid & is water-soluble; it’s unsurprising that glycogen itself contains a lot of water. In fact, it’s stored in liquid form; three to four parts water to one part glycogen (sources state 3-4g water to 1g glycogen).
When you restrict carbohydrate, you stop consuming glucose, the raw-material from which glycogen is made (see Fuel versus Energy for more details). Your stores of glycogen therefore deplete as your body burns energy, and because glycogen carries 3-4 parts water; your body loses a heck of a lot of liquid with it! This is the reason why weight-loss is often rapid at the start of a LCHF diet. You’re shipping the water stored alongside glycogen; and water is quite heavy!
What’s this got to do with salt?
We’ve identified that depleting glycogen stores also ships water. How is that water excreted? Predominantly in your urine.
Salt is vital to the body for survival; so important in fact that your tongue has special ‘salt-sensors’ in it, to detect its taste and prompt you to add more if levels are insufficient. If something is especially salty, your body prompts you to drink. This is why many pubs offer salty snacks such as peanuts or crisps – they want you to drink more! A high concentration of electrolytes in the body triggers our thirst mechanism – salt is an electrolyte!
So in entering a state of ketosis, your body is excreting water and salt through the depletion of glycogen. If high salt-levels trigger the thirst mechanism, but salt-levels are going down (as is water); it naturally follows that the thirst-mechanism is not sufficiently triggered to cover this water-loss. Our body’s water-balance gets temporarily thrown out of sync and we become dehydrated. This combination of mineral-deficiency and dehydration can leave you feeling incredibly nauseous, tired, weak and highly prone to headaches.
There is something else to throw into the mix – insulin.
This is a very difficult thing for a lay-person to research. The science is prohibitively complex and the information tends not to deal directly with this subject; rather simply referring to it as an aside.
One of the lesser known functions of insulin is to signal salt-retention in the kidneys. When you eat carbohydrate, your insulin levels rise. The insulin then tells your kidneys to retain salt and not excrete it. By eating carbohydrate, we’re not only getting fatter, but the salt we eat is not being released by the body, which then has adverse effects on blood-pressure. A low-salt diet can also lead to insulin-resistance, the precursor to type-2 diabetes (your body no longer responds to the insulin you produce).
Conversely, when you cut carbs; your insulin-levels decrease, which then tells your kidneys to release salt. The healthy ‘salt-cycle’ is restored and the body slowly adjusts to its normal, natural pattern.
In addition to water-loss through glycogen-depletion; insulin-reduction tells your kidneys to release salt from the body. For these two reasons, it’s important to up your salt in-take when first adopting a ketogenic-diet.
To prevent dehydration and the above symptoms (sometimes termed ‘keto-flu’), remember to drink lots of water and top your sodium levels up by drinking bouillon (stock cubes in water) and adding sufficient salt to your meals to cover the loss.
That way, your changeover to a healthy keto-plan will be a happy and safe one. Enjoy the journey!
I hope this helps and thanks for reading,
Adam.
country walks in ketosis 
I has a tummy bug this week and could not eat for three days. I was drinking as much as I was able to, but the headache that developed was crippling. I was thinking about you and the keto headaches with a great deal of sympathy!
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You seem to be saying that the salt depletion is temporary? Once established in ketosis should we return to a no-too-salty diet?
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Hi Bella, thank you for the comment. I caveat my response with the assertion that I’m in no way a medical professional; my view point comes from extensive reading around the subject, from all perspectives; those who criticise a keto-lifestyle; plus those who are heavyly for it!! To answer your question, “One of the lesser known functions of insulin is to signal salt-retention in the kidneys. When you eat carbohydrate, your insulin levels rise. The insulin then tells your kidneys to retain salt and not excrete it.” This means that as soon as your insulin levels increase [prompted by carbohydrate intake], your kidneys will start RETAINING salt, which is the unhealthy and dangerous thing. If you’re in ketosis, your insulin levels will be low and your kidneys will therefore NOT be receiving that message. Your natural electrolyte balance will kick in, and your kidneys will send the message to excrete the salt rather than retain it. This means that as long as you’re in ketosis, your body will happily regulate its own salt balance and there’s no need to worry about it. The ‘temporary’ part is that in the period of adjustment; your body is switching from one fuel source to another. It finds this HIGHLY confusing and that’s why people can often feel fairly terrible. Your body gets a little messed up when it doesn’t know where its energy is coming from and that ‘messed up feeling’ equally applies to salt. Your body has a temporary adjustment period where electrolyte regulation goes a little off kilter! So yes; the salt depletion is temporary, in the period that your body is adjusting to burning ketones. Once that has happened, you won’t experience salt depletion; nor do you have to worry about salty foods. Your body will regulate itself; taking what salt it needs and then naturally excreting the rest. A win win situation! Hop[e that helps and thanks again for the comment. Adam.
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Thanks Adam. That sounds good, I like not having to worry about salt, but not sure yet whether to give up( worrying that is)
I have hyperaldosteronism, too much of a hormone that controls blood pressure by regulating salt and potassium. I’m at risk of too much salt and too little potassium, and thereby high blood pressure. I am prescribed a diuretic that keeps the Potassium on board, but I’ve no idea about salt, except I see others with the condition encouraged to consume as little as possible. I shall ask around more to see whether ketosis would help us so salt monitoring is less of a problem, and I can enjoy pork scratching without fear or guilt! Do t worry I’m not holding you responsible for advice with an abnormality to consider!
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Keto/low carb is good to fight this underdiagnosed airborne infectious disease that can cause malignancies, precancerous conditions, rheumatological diseases, connective tissue diseases, heart disease, autoimmune symptoms, inflammation in any organ/tissue, adrenal insufficiency, seizures, migraines, hallucinations, etc. and is often undiagnosed/misdiagnosed in immunocompetent people. 80-90+% of people in some areas have been infected, and it can lay dormant for up to 40 years in the lungs and/or adrenals.
My coworkers and I, all immunocompetent, got Disseminated Histoplasmosis in Dallas-Fort Worth from roosting bats, the most numerous non-human mammal in the U.S., that shed the fungus in their feces. The doctors said we couldn’t possibly have it, since we all had intact immune systems. The doctors were wrong. Healthy people can get it, too. And we did not develop immunity over time. We’d get better and then progressively worse, relapsing periodically and concurrently every year.
More than 100 outbreaks have occurred in the U.S. since 1938, and those are just the ones that were figured out, since people go to different doctors. One outbreak was over 100,000 victims in Indianapolis.
It’s known to cause hematological malignancies, and doctors claim leukemia patients go into remission when given antifungal. My friend in another state who died from lupus lived across the street from a bat colony. An acquaintance with alopecia universalis and whose mother had degenerative brain disorder has bat houses on their property.
Researchers claim the subacute type is more common than believed. It’s known to at least “mimic” autoimmune diseases and cancer and known to give false-positives in PET scans. But no one diagnosed with an autoimmune disease or cancer is screened for it. In fact, at least one NIH paper states explicitly that all patients diagnosed with sarcoidosis be tested for it, but most, if not all, are not. Other doctors are claiming sarcoidosis IS disseminated histoplasmosis.
What if this infection, that made me and my coworkers so ill, isn’t rare in immunocompetent people? What if just the diagnosis is rare, since most doctors ignore it? Especially since online documents erroneously state it’s not zoonotic.
Older documents state people who spend a lot of time in a building with roosting bats, in caves, working as landscapers, construction workers, pest control workers, etc. are known to get Disseminated Histoplasmosis, but the info appears to have been lost, for the most part. And now bat conservationists encourage people to leave bats in buildings/homes. What a terrible mistake they’ve made.
This pathogen parasitizes the reticuloendothelial system/invades macrophages, can infect and affect the lymphatic system and all tissues/organs, causes inflammation, granulomas, and idiopathic (unknown cause) diseases and conditions, including hematological malignancies, autoimmune symptoms, myelitis, myositis, vasculitis, panniculitis, dysplasia, hyperplasia, etc. It causes hypervascularization, calcifications, sclerosis, fibrosis, necrosis, eosinophilia, leukopenia, anemia, neutrophilia, pancytopenia, thrombocytopenia, hypoglycemia, cysts, abscesses, polyps, stenosis, perforations, GI problems, hepatitis, focal neurologic deficits, etc.
Many diseases it might cause are comorbid with other diseases it might cause, for example depression/anxiety/MS linked to Crohn’s.
The fungus is an Oxygenale and therefore consumes collagen. It’s known to cause connective tissue diseases (Myxomatous degeneration?), rheumatological conditions, seizures, and mental illness. Fungal hyphae carry an electrical charge and align under a current. It causes RNA/DNA damage. It’s known to cause delusions, wild mood swings (pseudobulbar affect?), and hallucinations. It’s most potent in female lactating bats, because the fungus likes sugar (lactose) and nitrogen (amino acids, protein, neurotransmitters?), releasing lactase and proteinases to obtain them. What about female lactating humans…postpartum psychosis (and don’t some of these poor women also have trouble swallowing)? The bats give birth late spring/summer, and I noticed suicide rates spike in late spring/early summer. It’s known to cause retinal detachment, and retinal detachments are known to peak around June-July/in hot weather. A map of mental distress and some diseases appear to almost perfectly overlay a map of Histoplasmosis. Johns Hopkins linked autism to an immune response in the womb. Alzheimer’s was linked to hypoglycemia, which can be caused by chronic CNS histoplasmosis. Cancer is known to occur more often near rivers than in mountains or deserts, just like this infection.
The bats eat moths, which are attracted to blue and white city lights that simulate the moon the moths use to navigate. Bats feed up to 500 feet in the air and six miles away in any direction from their roost, but not when it’s raining or when the temperature is less than approximately 56° F. The fungus can grow in bird feces, but birds don’t carry it because their body temperature is too high, killing the fungus.
I believe the “side effects” of Haldol (leukopenia and MS symptoms) might not always be side effects but just more symptoms of Disseminated Histoplasmosis, since it causes leukopenia and MS symptoms. What about the unknown reason why beta receptor blockers cause tardive dyskinesia? The tinnitus, photophobia, psychosis “caused” by Cipro? Hypersexuality and leukemia “caused” by Abilify? Humira linked to lymphoma, leukemia and melanoma in children? Disseminated Histoplasmosis is known to cause enteropathy, so could some people thought to have nonsteroidal anti-inflammatory drug enteropathy have it and taking NSAIDs for the pain/inflammation it causes, and the NSAIDs aren’t the actual culprit?
From my experience, I learned that NO doctor, at least in DFW, will suspect subacute and/or progressive disseminated histoplasmosis in immunocompetent people. Some doctors, at least the ones I went to, will actually REFUSE to test for it, even when told someone and their coworkers have all the symptoms and spend a lot of time in a building with bats in the ceiling. Victims will be accused of hypochondriasis. (My doctors told me only farmer’s get it, it’s only in bird feces, and it only infects the lungs…wrong, wrong, and wrong!) In fact, the first doctor to diagnose me was a pulmonologist, and the only reason he examined me was to try to prove that I didn’t have it, when I really did. No doctor I went to realized bats carry the fungus. And NO doctor I went to in DFW, even infectious disease “experts,” understand the DISSEMINATED form, just the pulmonary form, and the only test that will be done by many doctors before they diagnose people as NOT having it is an X-ray, even though at least 40-70% of victims will have NO sign of it on a lung X-ray. It OFTEN gives false-negatives in lab tests (some people are correctly diagnosed only during an autopsy after obtaining negative test results) and cultures may not show growth until after 6-12 weeks of incubation (but some labs report results after 2 weeks).
One disease of unknown cause that could be caused by Disseminated Histoplasmosis: I suspect, based on my and my coworker’s symptoms (during our “rare” infectious disease outbreak) and my research, that interstitial cystitis and its comorbid conditions can be caused by disseminated histoplasmosis, which causes inflammation throughout the body, causes “autoimmune” symptoms, and is not as rare as believed. I read that “interstitial cystitis (IC) is a chronic inflammatory condition of the submucosal and muscular layers of the bladder, and the cause is currently unknown. Some people with IC have been diagnosed with other conditions such as irritable bowel syndrome (IBS), fibromyalgia, chronic fatigue syndrome, allergies, and Sjogren’s syndrome, which raises the possibility that interstitial cystitis may be caused by mechanisms that cause these other conditions. In addition, men with IC are frequently diagnosed as having chronic nonbacterial prostatitis, and there is an extensive overlap of symptoms and treatment between the two conditions, leading researchers to posit that the conditions may share the same etiology and pathology.” Sounds like Disseminated Histoplasmosis, doesn’t it?
My coworkers and I were always most ill around April/May/June, presumably since the Mexican Free-tail bats gave birth in Texas during May (and the fungus was most potent), and fall/Thanksgiving to December, for some unknown reason (maybe migrating bats from the north?). We had GI problems, liver problems, weird rashes (erythema nodosum, erythema multiforme, erythema marginatum/annulare, etc.), plantar fasciitis, etc., and I had swollen lymph nodes, hives, lesions, abdominal aura, and started getting migraines and plantar fasciitis in the building, and I haven’t had them since I left. It gave me temporary fecal incontinence, seizures, dark blood from my intestines, tinnitus, nystagmus, blurry vision/floaters/flashes of light, benign paroxysmal positional vertigo, isolated diastolic hypertension, what felt like burning skin, various aches and pains (some felt like pin pricks and pinches), tingling, tremors, “explosions” like fireworks in my head while sleeping, and temporary blindness. Suddenly I was allergic to Comice pears (latex fruit allergy or oral allergy syndrome?). I had insomnia (presumably from the fungus acidifying the blood, releasing adrenaline) and parasomnias. It felt like strong bursts of electrical shocks or steady electrical currents in my body, which now feel like low electrical currents at times, mostly at night. I suddenly had symptoms of several inflammatory/autoimmune diseases, including Fibromyalgia, Sarcoidosis, ALS, MS, Sjogren’s syndrome, etc. that have disappeared since leaving the area and taking nothing but Itraconazole antifungal.
No one, including doctors (we all went to different ones), could figure out what was wrong with us, and I was being killed by my doctor, who mistakenly refused to believe I had it and gave me progressively higher and higher doses of Prednisone (2 years after I already had Disseminated Histoplasmosis) after a positive ANA titer, until I miraculously remembered that a visiting man once told my elementary school class that bats CARRY histoplasmosis. So much of it that they evolved to deal with the photophobia and tinnitus it causes by hunting at night by echolocation. There’s a lot more. I wrote a book about my experience with Disseminated Histoplasmosis called “Batsh#t Crazy,” because bats shed the fungus in their feces and it causes delusions and hallucinations, I suspect by the sclerotia fungal mycelia can form emitting hallucinogens (like psilocybin and dimethyltryptamine) along with inflammation in the CNS. (Schizophrenics have 2X of a chemical associated with yeast, part of the fungal life cycle.)
Thank you for your time,
Susan McIntyre
P.S. Doesn’t this infection share all the same symptoms with Gulf War Syndrome?
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