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Archived Comments for: Ketoacidosis associated with low-carbohydrate diet in a non-diabetic lactating woman: a case report

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  1. Comment on ”Ketoacidosis associated with low-carbohydrate diet in a non-diabetic lactating woman: a case report"

    Csaba Tóth, Paleomedicina Hungary Ltd., Budapest, Hungary

    20 October 2015

    I became curious when I read the title of the case report by drs. Geijer and Ekelund. I am using a low carbohydrate diet, we refer to as the paleolithic ketogenic diet, in the treatment of diverse chronic diseases already for six years [1-6]. I have to say that in my practice I did never see a single case where ketoacidosis or metabolic acidosis developed while on the paleolithic ketogenic diet, even though I am familiar with the diagnosis and treatment of these conditions given my 5-years experience in ICU.

    In my reply I would like to comment on the case presented and to clarify some common misunderstandings related to ketosis which are also reflected in this report.

    First, lactation itself does not predispose to ketosis. Whether ketosis develops in a healthy lactating woman only depends on the type of the nutrition. In newborn infants, however, ketosis is achieved within a few hours after birth and they remain so while breastfeeding. There is ample evidence showing that the state of ketosis is not abnormal but physiological at any age. For example, indigenous people of the Arctic following a traditional fat-meat based diet containing little or no carbohydrate are in ketosis through their entire lifespan. Our experience with patients also indicates that even a prolonged full fat-meat diet does neither predispose to ketosis or metabolic acidosis. Given these facts the explanation for the phenomenon described in the report of drs. Geijer and Ekelund lies elsewhere.

    It is important to emphasize that low carbohydrate diets can only be maintained on the long term when the diet is high in fat. Yet, in the case report it is not detailed how the authors ascertained whether the diet was indeed high in fat and what exactly the patient was eating. Other important details were not mentioned either such as the weight or BMI of the patient. This is an important issue given that loss of 4 kg within 10 days in a thin patient should be regarded as starvation. In an obese patient, however, such a weight loss simply reflects loss of retained water but not starvation. It is also not mentioned whether breath acetone was detectable or not, an important characteristic of ketoacidosis.

    In the following I put forward those possible scenarios which alone or in combination may explain the development of the condition described in the patient.


    1. Any diet with low fat-low carbohydrate content

    Given the unreliable sources on the internet, lack of full appreciation of nutrition basics, lack of professional guidance as well as fear from fats, it may occur that a patient on a low carbohydrate diet does not eat fat in enough quantities. Given that energy comes either from fat or glucose these patients are indeed starving. Low fat-low carbohydrate diets are not sustainable on the long term. This is especially the case in lean patients with low fat reserves. This condition may lead to mild acidosis and some of the symptoms mentioned in the report.


    2. The classical ketogenic diet

    The classical ketogenic diet (and some close variants) has long been used for nearly a century in the treatment of epilepsy and thus considerable experience has been gathered with its use. It is well-recognized that the classical ketogenic diet is associated with side effects some of which were also seen in this patient including mild acidosis, nausea, vomiting, cramps and malaise. Importantly, in the classical ketogenic diet the blood ketone concentration desired for adequate epilepsy control is above 6 mmol/l which is quite close to the 7.1 mmol/l ketone concentration of the patient. In the ketogenic diet literature there is general agreement that only ketone concentrations above 15 mmol/l are regarded as cause for concern for severe metabolic acidosis [7]. It is also important to mention that side effects of the classical ketogenic diet (and also in the majority of the popular low carbohydrate diets) are not coming from ketosis but dietary components (unhealthy vegetable oils, either polyunsaturated or saturated, and dairy).


    3. Consumption of foods (e.g. meat products) with additives

    Tachycardia and malaise may be caused by food additives including nitrites and nitrates as well as natrium glutamate. Nausea and womiting may also develop following increased intake of meat products contaminated with dioxin, an underestimated issue associated with products of the food industry.


    4. Abrupt shift toward a low carbohydrate diet

    Nausea, womiting, headache and alterations of blood gas (low grade acidosis) may also develop if one shifts toward a low carbohydrate diet from a high carbohydrate diet abruptly. Symptoms may persist for 5-10 days and then are resolving spontaneously. These transitory side-effects are well-known and are explained by the fact that adaptation to a fat-based metabolism, which involves the upregulation of some mitochondrial enzymes, takes some time. Given that in the present case only 10 days have passed since dietary shift this may point to an incomplete adaptation.


    5. Excessive carbohydrate intake following starvation or low carbohydrate diet

    The phenomenon that excessive carbohydrate intake following prolonged starvation may cause acidosis is well-documented and is explained by the relative shortage of insulin while in a fat-adopted state. In particular, such cases were observed after the second world war when the concentration camps were liberated, and those who had been starving before received larger amounts of carbohydrate. Abrupt carbohydrate load in these cases may cause acidosis, headache, vomiting and hypotonia. Even death in some cases. A similar, although less severe condition is seen in those pregnant women who previously had been following a low carbohydrate diet undergo glucose tolerance test as part of their routine screening. In these cases mild nausea, acidosis and resulting low blood glucose may emerge. Importantly, in the present case the measured low level of blood glucose does neither preclude carbohydrate intake given that, for example, fructose does not elevate blood glucose.


    I suppose that any of the above situations, but most probably the fifth one, may more parsimoniously explain the condition described in the patient as compared to low carbohydrate-high fat diet which has never been described to result in ketoacidosis in non-diabetic subjects. In addition it seems probable that the patient was consuming larger amounts of vegetable oils before admission to hospital. This is indicated by the constellation of low thyroid hormones but normal TSH. Starvation only should have resulted in low thyroid hormones along with low TSH. The link between vegetable oils and decreased thyroid hormones is well-described in the literature [8] and our experience indicates that this also applies to coconut oil which instead of animal fats is commonly advocated by low carbohydrate proponents. Hypothyreosis in the past medical history of the patient also points to increased regular intake of vegetable oils. Given that thyroid hormones affect the synthesis of proteins consumption of vegetable oils may decrease the synthesis of insulin and that of the proteins of mitochondrial enzymes. In the present case consumption of vegetable oil might have hindered adaptation to the low carbohydrate diet.

    I suppose that in the present case an adequate ratio of fat to protein and the exclusive use of animal fat might have been able to reverse the acidosis and associated symptoms. As detailed earlier consumption of vegetable oils may prolong time required to adaptation to a fat based metabolism. During this period the patient may feel fatigue and malaise and therefore may feel need to consume carbohydrates thinking to help the situation. However, an opposite effect may be achieved.




    1. Clemens Z, Kelemen A, Fogarasi A, Tóth C. Childhood absence epilepsy successfully treated with the paleolithic ketogenic diet. Neurol Ther. 2013;2:71–6.

    2. Tóth C, Clemens Z. Type 1 diabetes mellitus successfully managed with the paleolithic ketogenic diet. Int J Case Rep Images. 2014;5:699–703.

    3. Tóth C, Clemens Z. Successful treatment of a patient with obesity, type 2 diabetes and hypertension with the paleolithic ketogenic diet. Int J Case Rep Images. 2015;6:161–167.

    4. Tóth C, Clemens Z. Gilbert’s syndrome successfully treated with the paleolithic ketogenic diet. Am J Med Case Rep. 2015;3:117–120.

    5. Clemens Z, Kelemen A, Tóth C. NREM-sleep Associated Epileptiform Discharges Disappeared Following a Shift toward the Paleolithic Ketogenic Diet in a Child with Extensive Cortical Malformation. Am J Med Case Rep. 2015;3:212–215.

    6. Clemens Z, Dabóczi A, Tóth C. The paleolithic ketogenic diet may ensure adequate magnesium levels. Med Hyp. 2015 (accepted for publication)

    7. Volek SF, Phinney SD. The art and science of low carbohydrate performance. Beyond Obesity LLC 2011

    8. Vazquez JA, Kazi U, Madani N. Protein metabolism during weight reduction with very-low-energy diets: evaluation of the independent effects of protein and carbohydrate on protein sparing. Am J Clin Nutr. 1995;62:93–103.

    Competing interests

    No competing interests
  2. Vegetable oils cause low thyroid?

    Leila Las, Universidade de São Paulo

    15 December 2015

    I could not agree more to the comment made by dr Toth, in every point made. There is, however, one single exception: the reference [8] does not support the statement that intake of vegetable oils would lower thyroid function. And most of all, maybe reduce the statement to multiply unsaturated fatty acids? Do you have evidence that it applies to all vegetable oils? Is the source (vegetable/animal) what counts or rather the fatty acid composition?

    Competing interests