ArticlePDF Available

Abstract and Figures

Introduction: Type 1 diabetes mellitus (T1DM) patients are usually instructed to follow a low fat/high carbohydrate diet. A few studies in literature, however, reported metabolic benefits and sustainability of carbohydrate restricted diets. Case Report: Herein, we present a case of a 19-year-old male with newly diagnosed T1DM. The patient was first put on an insulin regime. Twenty days later, he shifted towards the paleolithic ketogenic diet and was able to discontinue insulin. Strict adherence to the diet resulted in normal glucose levels and a more than three-fold elevation of C-peptide level indicating restored insulin production. Currently, the patient is on the paleolithic ketogenic diet for 6.5 months. He is free of complaints, and no side effects emerged. Conclusion: We conclude that the paleolithic ketogenic diet was effective and safe in the management of this case of newly diagnosed T1DM. Marked increase in C peptide level within two months indicates that the paleolithic ketogenic diet may halt or reverse autoimmune processes destructing pancreatic beta cell function in T1DM.
Content may be subject to copyright.
International Journal of Case Reports and Images, Vol. 5 No. 10, October 2014. ISSN – [0976-3198]
Int J Case Rep Images 2014;5(10):699–703.
Tóth et al. 699
Type 1 diabetes mellitus successfully managed with the
paleolithic ketogenic diet
Csaba Tóth, Zsófia Clemens
Introduction: Type 1 diabetes mellitus (T1DM)
patients are usually instructed to follow a low
fat/high carbohydrate diet. A few studies in
literature, however, reported metabolic benefits
and sustainability of carbohydrate restricted
diets. Case Report: Herein, we present a case
of a 19-year-old male with newly diagnosed
T1DM. The patient was first put on an insulin
regime. Twenty days later, he shifted towards
the paleolithic ketogenic diet and was able to
discontinue insulin. Strict adherence to the diet
resulted in normal glucose levels and a more than
three-fold elevation of C-peptide level indicating
restored insulin production. Currently, the
patient is on the paleolithic ketogenic diet for
6.5 months. He is free of complaints, and no
side effects emerged. Conclusion: We conclude
that the paleolithic ketogenic diet was effective
and safe in the management of this case of newly
diagnosed T1DM. Marked increase in C peptide
level within two months indicates that the
paleolithic ketogenic diet may halt or reverse
autoimmune processes destructing pancreatic
beta cell function in T1DM.
Keywords: Type 1 diabetes mellitus, Ketogenic
diet, Paleolithic-ketogenic diet, C-peptide,
Evolutionary medicine
Csaba Tóth1, Zsófia Clemens2
Affiliations: 1MD, Medical Director, Paleomedicina Hungary
Ltd, Evolutionary Medicine Working Group, Hidász u. 3,
H-1026, Budapest, Hungary; 2PhD, Senior Research Fellow,
Department of Neurology, University of Pécs, Rét u. 2,
H-7623, Pécs, Hungary.
Corresponding Author: Zsófia Clemens, Department of
Neurology, University of Pécs, Rét u. 2, H-7623, Pécs, Hungary.
Ph: 003672535900; Email:
Received: 08 July 2014
Accepted: 31 July 2014
Published: 01 October 2014
How to cite this article
Tóth C, Clemens Z. Type 1 diabetes mellitus
successfully managed with the paleolithic ketogenic
diet. Int J Case Rep Images 2014;5(10):699–703.
Diabetic patients are, generally, recommended to
follow a diet that is low in fat and high in carbohydrates
[1]. Clinical studies, conversely, showed metabolic
benefits conferred by carbohydrate-restricted diets
including the ketogenic diet [2, 3] and the paleolithic
diet [4, 5] in type 2 diabetes. Much less data on the use
of low carbohydrate diets in type 1 diabetes (T1DM)
are available. Two studies by Nielsen et al. showed that
a low carbohydrate diet lowers the need for insulin as
well as the number of hypoglycemic episodes in T1DM
[6, 7]. It was also suggested that a low carbohydrate diet
is sustainable on the long-term [6, 7]. Ketogenic diets
have long been used in epilepsy [8]. There are three
cases in literature, where concurrent epilepsy and T1DM
were treated with the classical ketogenic diet and both
conditions improved [9–11]. Recently, we published
a case of childhood absence epilepsy where seizure
freedom was achieved using a modified ketogenic diet we
refer to as the paleolithic-ketogenic diet [12]. Herein, we
present a case of T1DM, where the same diet resulted in
remission of T1DM as assessed by normalization of blood
glucose levels and elevation in C-peptide level allowing
for discontinuation of external insulin replacement.
A 19-year-old male complained of increased thirst,
polyuria, itchy skin, malaise, and weight loss. The
symptoms were present for about two weeks prior to
International Journal of Case Reports and Images, Vol. 5 No. 10, October 2014. ISSN – [0976-3198]
Int J Case Rep Images 2014;55(10):699–703.
Tóth et al. 700
diagnosis. On November 24, 2013 self monitoring of
blood glucose showed 384 mg/dL. Previous medical
history was unremarkable. Anamnestic data included
consuming of muscle boosting protein through a month
prior to symptom onset. Laboratory assessment on
November 25, 2013 (Table 1) showed elevations in glucose
(218 mg/dL) and HbA1c (9.2%). Testing for glutamic acid
decarboxylase (GAD) antibodies showed positivity
(52 U/mL; normal range 0–10 U/mL) and mild positivity
for pancreatic islet cell autoantibodies (ICAs). C-peptide
level was not measured at this time. He was diagnosed
with T1DM. He was put on insulin replacement therapy
(38 IU of insulin) and standard conventional diabetes
diet with six meals containing 240 grams carbohydrate
daily. He followed this regime for 20 days. While on this
regime his glucose levels fluctuated between 68–267
mg/dL (Figure 1).
Carbohydrate he consuming before was less than 240
grams. Since his malaise did not improve the patient
consulted the first author in December 2013. To ascertain
T1DM laboratory examination of C-peptide was carried
out. C-peptide level of 0.6 ng/mL measured on January
08, 2014 indicated subnormal insulin secretion (Figure
2). The patient was suggested to switch to the paleolithic-
ketogenic diet which he initiated on December 21, 2013.
From this time, he was also taking 5,000 IU of vitamin
D3 but nothing else as supplement. His diet consisted
of meat, organ meat, fat and eggs. In his diet, red and
fat meats dominated over lean meats. He was eating
vegetables in insignificant amounts. His diet had a
ketogenic ratio (fat : protein + carbohydrate) of at least
2:1. No oil of plant origin or artificial sweeteners were
allowed. The patient was under our close control and
reported daily food records and blood glucose levels.
Upon shifting toward the paleolithic ketogenic diet
glucose levels returned to normal and no major elevations
were seen postprandially either. Insulin was therefore
discontinued. The tapering of insulin was done promptly:
following the first paleolithic-ketogenic meal glucose level
was only 86 mg/dL thus there was no need for external
insulin. Similar blood glucose levels were measured on
subsequent meals on the diet. Thus, the patient required
no insulin subsequently either. Home glucose monitoring
was carried out preprandially as well as postprandially
and tracked once a day for consecutive meals (that is on
consecutive days measures were taken for breakfast, lunch
and dinner, respectively). Average blood glucose level
while on the standard diabetes diet with insulin was 119
mg/dL while 85 mg/dL on the paleolithic-ketogenic diet
without insulin. Fluctuations in glucose levels decreased
as indicated by a reduction of standard deviation values
from 47 mg/dL on the standard diabetes diet to 9 mg/dL
on the paleolithic-ketogenic diet. Average postprandial
glucose elevation on the standard diabetes diet was 23
mg/dL while only 5.4 mg/dL on the paleolithic-ketogenic
diet (Figure 1).
C-peptide measurement was repeated on the 10th
week of the diet (on March 06, 2014). This indicated
an elevation to a value of 2.2 ng/mL (Figure 2). A
comprehensive laboratory workup carried out on March
14, 2014 indicated normal laboratory parameters with
the exception of total cholesterol and LDL cholesterol
which were slightly elevated. Glucose level was 88 mg/
dL while HbA1c was 5.5% (for all laboratory values see
Table 1). Urinary ketone was positive. On March 21, 2014
antibody testing for ICA showed no change in the mild
Table 1: Laboratory data at the time of diagnosis on a normal diet
(on November 25, 2013) and at 10 weeks after diet initiation,
on the paleolithic-ketogenic diet without insulin (on March 14,
2014). Note the normal level of glucose, HbA1c and low level
of triglyceride while on the paleolithic-ketogenic diet. Dashes
indicate that the given parameter was not measured.
Normal diet Paleolithic-ketogenic diet
WBC 5.9 5.4 G/l
RBC 5.7 5.3 T/l
Hemoglobin 16 15.2 G/dL
Hematocrit 48 45 %
Iron 136.3 98.9 µg/ dL
Thrombocyte 230 150 G/l
Sodium 134 139 mEq/l
Potassium 3.9 3.8 mEq/l
Calcium 9.52 10 mg/dL
Magnesium 2.02 mg/dL
Carbamide 10.6 14.8 mg/dL
Creatinine 0.88 0.97 mg/dL
eGFR >90 >90
Glucose 218 88 mg/dL
Hb1Ac 9.2 5.5 %
Total cholesterol 143 301 mg/dL
HDL cholesterol 54.8 mg/dL
LDL cholesterol 224 mg/dL
Triglyceride 168 111 mg/dL
Uric acid 6.12 mg/dL
GOT 31 19 U/l
GPT 44 18 U/l
GGT 17 16 U/l
Total bilirubin 0.94 mg/dL
TSH 3.53 mIU/l
CRP 1.1 mg/L
Abbreviations: WBC - white blood cell count, RBC - red blood
cell count, eGFR - estimated glomerular filtration rate, HbA1c -
glycated hemoglobin, HDL - high density lipoprotein, LDL - low
density lipoprotein, TSH - thyroid stimulating hormone, CRP
- C-reactive protein
International Journal of Case Reports and Images, Vol. 5 No. 10, October 2014. ISSN – [0976-3198]
Int J Case Rep Images 2014;55(10):699–703.
Tóth et al. 701
positivity measured before and some elevation in GAD
antibodies (86 U/mL). At the time of writing this case
report, the patient is on the paleolithic ketogenic diet for
6.5 months and still exhibit low glucose levels. No side
effects emerged and he is completely free of symptoms.
The patient gave written informed consent for writing
this case study.
This is a first report of T1DM being successfully
managed with the paleolithic-ketogenic diet. In literature,
a few studies are available on the use of carbohydrate
restricted diet in the treatment of T1DM [6, 7]. Low
carbohydrate diet in these studies resulted in reduced
number of hypoglycemic episodes and also lowered
the need for insulin. In our case, however, insulin
replacement was not just reduced but could be stopped.
Importantly, insulin discontinuation was paralleled by
a marked increase in C peptide level indicating restored
pancreatic insulin production.
Shortly before diabetes onset our patient consumed
muscle boosting protein which contained bovine milk
protein. Consumption of cow’s milk has repeatedly been
shown to increase risk of T1DM [13, 14]. It is suggested
that bovine milk protein may promote autoimmune
processes giving rise to T1DM [15]. Also in two case
reports from literature, where epilepsy was treated
with the classical ketogenic diet, which contains large
amount of dairy, T1DM developed subsequently [9, 11].
A major difference between the classical ketogenic diet
and the paleolithic ketogenic diet is that milk and dairy
are excluded in the latter. We suggest that the paleolithic
ketogenic diet not only normalize glucose levels but
may also halt autoimmune processes mediated by non-
paleolithic substances including milk protein [16].
While on the paleolithic-ketogenic diet glucose levels
remained low both during preprandially and postprandially.
Follow-up laboratory assessment indicated laboratory
parameters remaining in the normal range except for
elevations in total cholesterol and LDL cholesterol. In fact,
these elevations are expected on a diet rich in animal fat
and cholesterol and were also reported in studies with the
classical ketogenic diet [17] as well as in our previous case
of childhood absence epilepsy treated with the paleolithic
ketogenic diet [12]. Moreover, it is now acknowledged that
neither dietary nor serum cholesterol represent a risk factor
for cardiovascular disease [18]. On follow-up antibody
testing ICA remained mildly positive while GAD antibodies
elevated to some extent. Although these parameters are
frequently associated with T1DM they do not seem to be
specific nor indicate progression of disease [19].
Type 1 diabetes mellitus is considered as a lifelong
metabolic condition due to the exhaustion of insulin-
secretory cells of the pancreas. Therefore, T1DM is
generally believed to be untreatable by any diet. There
are indications, however, that residual pancreatic beta
cell functioning may extend well beyond the time of
diagnosis [20]. Nevertheless C-peptide levels decrease
monotonically through years after diagnosis [20]. We are
not aware of any data from literature indicating elevation
of C-peptide resulting from a dietary intervention. A
recent case study of a child with T1DM reported remission
without insulin on gluten-free diet [21]. However, in that
case C-peptide continued to decline while on the gluten-
free diet.
Figure 1: Blood glucose levels while on the standard diabetes
diet containing 240 g carbohydrate with insulin therapy and
while on the paleolithic-ketogenic diet without insulin. Glucose
was measured preprandially and postprandially once a day for
consecutive meals (that is on consecutive days measures were
taken for breakfast, lunch and dinner, respectively). Note low
glucose levels and the absence of major postprandial elevations
while on the paleolithic ketogenic diet. Due to stable glucose
levels through five months, from May 15, 2014 the patient
switched to self-monitoring his glucose levels only once a week.
Figure 2: C-peptide levels shortly after diet initiation (on the
18th day of the paleolithic ketogenic diet) and two months later.
Note the more than three-fold increase in C-peptide within two
International Journal of Case Reports and Images, Vol. 5 No. 10, October 2014. ISSN – [0976-3198]
Int J Case Rep Images 2014;55(10):699–703.
Tóth et al. 702
In the standard care of T1DM insulin is a cornerstone.
It is important to emphasize that the paleolithic-
ketogenic diet as a standalone therapy may be applied
only in those cases with residual insulin secretion. In
cases with no internal insulin secretion the paleolithic-
ketogenic therapy may be only used as an adjunct to
insulin replacement.
We suggest that an intervention with the paleolithic
ketogenic diet in an early stage of the disease with residual
insulin secretion may halt or reverse type 1 diabetes
mellitus (T1DM). Follow-up at sixth month in the case of
our patient is relatively short and the positive results may
appear as a honeymoon effect. However, this term is used
in relation to the beginning of insulin therapy not the end
of it. We believe that with normalized insulin secretion
and a further adherence to the diet the patient may be
managed on the long-term.
Author Contributions
Tóth Csaba – Substantial contributions to conception and
design, Acquisition of data, Analysis and interpretation
of data, Drafting the article, Revising it critically for
important intellectual content, Final approval of the
version to be published
Zsófia Clemens – Substantial contributions to
conception and design, Acquisition of data, Analysis
and interpretation of data, Drafting the article, Revising
it critically for important intellectual content, Final
approval of the version to be published
The corresponding author is the guarantor of submission.
Conflict of Interest
Authors declare no conflict of interest.
© 2014 Tóth Csaba et al. This article is distributed
under the terms of Creative Commons Attribution
License which permits unrestricted use, distribution
and reproduction in any medium provided the original
author(s) and original publisher are properly credited.
Please see the copyright policy on the journal website for
more information.
1. Bantle JP, Wylie-Rosett J, Albright AL, et al. Nutrition
recommendations and interventions for diabetes:
A position statement of the American Diabetes
Association. Diabetes Care 2008 Jan;31 Suppl 1:S61–
2. Mobbs CV, Mastaitis J, Isoda F, Poplawski M.
Treatment of diabetes and diabetic complications with
a ketogenic diet. J Child Neurol 2013;28(8):1009–4.
3. Yancy WS Jr, Foy M, Chalecki AM, Vernon MC,
Westman EC. A low-carbohydrate, ketogenic diet to
treat type 2 diabetes. Nutr Metab (Lond) 2005;2:34.
4. Jönsson T, Granfeldt Y, Ahrén B, et al. Beneficial
effects of a Paleolithic diet on cardiovascular risk
factors in type 2 diabetes: A randomized cross-over
pilot study. Cardiovasc Diabetol 2009;16;8:35.
5. Klonoff DC. The beneficial effects of a Paleolithic
diet on type 2 diabetes and other risk factors for
cardiovascular disease. J Diabetes Sci Technol
6. Nielsen JV, Jönsson E, Ivarsson A. A low carbohydrate
diet in type 1 diabetes: clinical experience--a brief
report. Ups J Med Sci 2005;110(3):267–3.
7. Nielsen JV, Gando C, Joensson E, Paulsson C.
Low carbohydrate diet in type 1 diabetes, long-
term improvement and adherence: A clinical audit.
Diabetol Metab Syndr 2012;4(1):23.
8. Kossoff EH, Rho JM. Ketogenic diets: Evidence for
short-and long-term efficacy. Neurotherapeutics
9. Henwood MJ, Thornton PS, Preis CM, Chee C,
Grimberg A. Reconciling diabetes management and the
ketogenic diet in a child with pyruvate dehydrogenase
deficiency. J ChildNeurol 2006;21(5):436–9.
10. Dressler A, Reithofer E, Trimmel-Schwahofer P, et al.
Type 1 diabetes and epilepsy: Efficacy and safety of
the ketogenic diet. Epilepsia 2010;51(6):1086–9.
11. Aguirre Castaneda RL, Mack KJ, Lteif A. Successful
treatment of type 1 diabetes and seizures with
combined ketogenic diet and insulin. Pediatrics
12. Clemens Z, Kelemen A, Fogarasi A, Tóth C. Childhood
Absence Epilepsy Successfully Treated with the
Paleolithic Ketogenic Diet. Neurology and Therapy
13. Elliott RB, Harris DP, Hill JP, Bibby NJ, Wasmuth
HE. Type I (insulin-dependent) diabetes mellitus and
cow milk: Casein variant consumption. Diabetologia
14. Wasmuth HE, Kolb H. Cow’s milk and immune-
mediated diabetes. Proc Nutr Soc 2000;59(4):573–9.
15. Sarugeri E, Dozio N, Meschi F, Pastore MR, Bonifacio
E. Cellular and humoral immunity against cow’s
milk proteins in type 1 diabetes. J Autoimmun 1999
16. Cordain L, Eaton SB, Sebastian A, et al. Origins and
evolution of the Western diet: Health implications for
the 21st century. Am J Clin Nutr 2005;81(2):341–54.
17. Liu YM, Lowe H, Zak MM, Kobayashi J, Chan VW,
Donner EJ. Can children with hyperlipidemia receive
ketogenic diet for medication-resistant epilepsy? J
Child Neurol 2013;28(4):479–83.
18. Lecerf JM, de Lorgeril M. Dietary cholesterol:
From physiology to cardiovascular risk. Br J Nutr
19. Jaeger C, Allendörfer J, Hatziagelaki E, et al.
Persistent GAD 65 antibodies in longstanding IDDM
are not associated with residual beta-cell function,
International Journal of Case Reports and Images, Vol. 5 No. 10, October 2014. ISSN – [0976-3198]
Int J Case Rep Images 2014;55(10):699–703.
Tóth et al. 703
neuropathy or HLA-DR status. Horm Metab Res
20. Wang L, Lovejoy NF, Faustman DL. Persistence of
prolonged C-peptide production in type 1 diabetes
as measured with an ultrasensitive C-peptide assay.
Diabetes Care 2012;35(3):465–70.
21. Sildorf SM, Fredheim S, Svensson J, Buschard K.
Remission without insulin therapy on gluten-free diet
in a 6-year old boy with type 1 diabetes mellitus. BMJ
Case Rep 2012.
Article citation: Tóth C, Clemens Z. Type 1 diabetes mellitus successfully managed with the paleolithic ketogenic
diet. Int J Case Rep Images 2014;5(10):699–703.
Csaba Tóth is General Practitioner from Hungary with 20 years experience in intensive care medicine,
internal medicine and family medicine. He is using the paleolithic-ketogenic nutrition in the treatment
of chronic medical illnesses including diabetes, cancer, autoimmune diseases and epilepsy for ve
years. He is operating private practice in Budapest and in a few other cities in Hungary. In 2013, he
organized a course on evolutionary medicine in the mandatory training of GPs at the University of
Szeged, Hungary. With an evolutionary medical attitude he strives for the full recovery of his patients.
Zsóa Clemens is Biologist and clinical researcher specialized in nutrition, nutritional therapy and
brain research. She earned her PhD in electroencephalograpy of sleep and epilepsy from Semmelweis
University, Budapest, Hungary in 2005. Currently, she is Senior Research Fellow at the Neurological
Department, University of Pécs, Hungary and is also afliated with the Evolutionary Medicine Working
Group of Paleomedicina Hungary Ltd. In international academic journals, she has published 29 research
articles with more than 500 citations. Email: clemenszso
Access full text article on
other devices
Access PDF of article on
other devices
Edorium Journals: On Web
About Edorium Journals
Edorium Journals is a publisher of high-quality, open ac-
cess, international scholarly journals covering subjects in
basic sciences and clinical specialties and subspecialties.
Edorium Journals
Edorium Journals et al.
Edorium Journals: An introduction
Edorium Journals Team
But why should you publish with Edorium
In less than 10 words - we give you what no one does.
Vision of being the best
We have the vision of making our journals the best and
the most authoritative journals in their respective special-
ties. We are working towards this goal every day of every
week of every month of every year.
Exceptional services
We care for you, your work and your time. Our efficient,
personalized and courteous services are a testimony to this.
Editorial Review
All manuscripts submitted to Edorium Journals undergo
pre-processing review, first editorial review, peer review,
second editorial review and finally third editorial review.
Peer Review
All manuscripts submitted to Edorium Journals undergo
anonymous, double-blind, external peer review.
Early View version
Early View version of your manuscript will be published
in the journal within 72 hours of final acceptance.
Manuscript status
From submission to publication of your article you will
get regular updates (minimum six times) about status of
your manuscripts directly in your email.
Our Commitment
Mentored Review Articles (MRA)
Our academic program “Mentored Review Article”
(MRA) gives you a unique opportunity to publish papers
under mentorship of international faculty. These articles
are published free of charges.
Favored Author program
One email is all it takes to become our favored author.
You will not only get fee waivers but also get information
and insights about scholarly publishing.
Institutional Membership program
Join our Institutional Memberships program and help
scholars from your institute make their research accessi-
ble to all and save thousands of dollars in fees make their
research accessible to all.
Our presence
We have some of the best designed publication formats.
Our websites are very user friendly and enable you to do
your work very easily with no hassle.
Something more...
We request you to have a look at our website to know
more about us and our services.
We welcome you to interact with us, share with us, join us and of course publish with us.
Browse Journals
Invitation for article submission
We sincerely invite you to submit your valuable
research for publication to Edorium Journals.
Six weeks
You will get first decision on your manuscript within six
weeks (42 days) of submission. If we fail to honor this
by even one day, we will publish your manuscript free
of charge.
Four weeks
After we receive page proofs, your manuscript will be
published in the journal within four weeks (31 days).
If we fail to honor this by even one day, we will pub-
lish your manuscript free of charge and refund you
the full article publication charges you paid for your
This page is not a part of the published article. This page is an introduction to Edorium Journals and the publication services.
... This is an animal fat-meat based diet similar to that originally proposed and used by gastroenterologist Voegtlin (13). To date we have published eight cases including patients with epilepsy (14,15), type 1 diabetes (16,17), metabolic syndrome (18), Gilbert's syndrome (19), Crohn's disease (20) and soft palate cancer (21) successfully treated with the paleolithic ketogenic diet. Importantly, the classic version of the ketogenic diet is known to be associated with low magnesium levels (22) one of the most well-known side-effects of the classic ketogenic diet. ...
... Importantly, the classic version of the ketogenic diet is known to be associated with low magnesium levels (22) one of the most well-known side-effects of the classic ketogenic diet. Our published cases (14)(15)(16)(17)(18)(19)(20)(21), along with our general experience, however, indicate that magnesium levels are normal on the paleolithic ketogenic diet. In order to quantify this clinical observation we performed a study in which we retrospectively assessed magnesium levels in relation to glycemic parameters in 45 patients with various diseases and five healthy subjects on the paleolithic ketogenic diet. ...
... were low. A similar pattern of laboratory parameters was seen in our previous case studies with the paleolithic ketogenic diet (14)(15)(16)(17)(18)(19)(20)(21) and may be regarded as indicating adequate dietary adherence. ...
Full-text available
Magnesium plays an essential role in several enzymatic reactions. Its deficiency is known to be widespread and has been associated with a variety of pathological conditions characterized by chronic inflammation and/or oxidative stress. The connection between the metabolism of glucose and magnesium at the cell level is wellestablished. We hypothesize that magnesium deficiency in chronic conditions is primarily due to Western type carbohydrate based metabolism. In previous case studies we have shown that magnesium levels are normal on the paleolithic ketogenic diet. Here we assessed magnesium levels in a larger sample (n=50) to address whether the paleolithic ketogenic diet is able to ensure normal blood magnesium levels. Materials and Methods To assess magnesium levels in patients and healthy controls on the paleolithic ketogenic diet in a larger sample, we retrospectively analysed laboratory data obtained from 50 patients/subjects who were following the diet and were also not taking magnesium or other supplements. Correlation calculation was performed between magnesium and glucose levels. Results We found magnesium levels to be in the normal range in all but one patient/subject. There was a significant inverse correlation between glucose and magnesium levels. Discussion Our results indicate that the paleolithic ketogenic diet ensures normal magnesium levels in various pathological conditions as well as in healthy subjects. We believe that the high prevelance of magnesium deficiency reported earlier for a variety of chronic conditions is correlated with carbohydrate-based Western type nutrition rather than that of the chronic condition itself. We discuss underlying mechanisms. Keywords magnesium, paleolithic, ketogenic, glucose, glycated hemoglobin, diabetesn
... Three major benefits are known to be associated with low carb (or ketogenic) diets: (1) glucose control, (2) decreasing insulin need and (3) decreasing the number of hypoglycemic episodes [1]. The PKD confers the same benefits in T1DM but in addition, it also ensures inflammation control [2,3] which is of utmost importance given the autoimmune origin of the disease. By controlling inflammation, the PKD likely prevents the development of long-term complications [4]. ...
... By controlling inflammation, the PKD likely prevents the development of long-term complications [4]. Moreover, in patients with new-onset T1DM, intervening with the PKD also results in preventing further decay of their own insulin production as shown by stable or even increased C-peptide measurements following a shift toward the PKD [2,3]. In the presentation we show six cases with T1DM where normoglycemia and long-term insulin freedom was achieved, along with preserved C-peptide production. ...
... It has been reported that high-carbohydrate diets can accelerate the death of the remaining islet cells in diabetic patients and Turk J Endocrinol Metab Bozbulut et al. 2019;23:112-121 Effects of a Low-Carbohydrate Diets on Type 1 Diabetes lead to a process called β-cell depletion (34). It has been shown that high levels of blood glucose reduce the ability of islet cells to produce insulin by inhibiting gene expression and binding to critical insulin transcription factors (42). It is suggested that these effects, together with the depletion of β-cells, may accelerate the destruction of islet cells, increase the requirement of insulin, and lead to poorer glycemic control. ...
... The researchers reported that a low-carbohydrate diet may halt or reverse the autoimmune process leading to the destruction of pancreatic β-cells. However, they emphasized that the paleolithic ketogenic diet could only be used in patients with residual insulin secretion as a single treatment option (42,43). Pediatric endocrinologists and dieticians in Australia and New Zealand reported a series of cases examining the effects of low-carbohydrate diets on the endocrine and metabolic outcomes in children with type 1 diabetes. ...
... In contrast, a low-fat, isoenergetic diet designed to provide no more than 20% energy from fat a day, together with supplementation of 1 g of fish oil, effectively attenuated disease activity in SLE patients (247). Although it is yet to be tested whether high fat/low carbohydrate ketogenic diets are beneficial in SLE patients, a potential positive effect of ketogenic diets has been reported for some autoimmune patients with MS (248) or T1D (249). Interestingly, a ketogenic diet may also provide supportive care for COVID-19 patients (250), reducing their need for the intensive care unit (251). ...
Full-text available
The immune system is an efficiently toned machinery that discriminates between friends and foes for achieving both host defense and homeostasis. Deviation of immune recognition from foreign to self and/or long-lasting inflammatory responses results in the breakdown of tolerance. Meanwhile, educating the immune system and developing immunological memory are crucial for mounting defensive immune responses while protecting against autoimmunity. Still to elucidate is how diverse environmental factors could shape autoimmunity. The emergence of a world pandemic such as SARS-CoV-2 (COVID-19) not only threatens the more vulnerable individuals including those with autoimmune conditions but also promotes an unprecedented shift in people’s dietary approaches while urging for extraordinary hygiene measures that likely contribute to the development or exacerbation of autoimmunity. Thus, there is an urgent need to understand how environmental factors modulate systemic autoimmunity to better mitigate the incidence and or severity of COVID-19 among the more vulnerable populations. Here, we discuss the effects of diet (macronutrients and micronutrients) and hygiene (the use of disinfectants) on autoimmunity with a focus on systemic lupus erythematosus.
... The child's daily average dosages of basal and rapid-acting insulin were reduced from 3.8 to 0.4 units, and from 1.4 to 0.7 units, respectively, with the use of a VLCD. Authors of another two studies suggested that, with the use of the palaeolithic-ketogenic diet, it was possible to completely withdraw insulin by extending the 'honeymoon period' (when the pancreas is still able to produce some insulin after blood sugar levels become nearly normal) (Tóth and Clemens, 2014;. Although no specific diet for people with diabetes exists, avoiding refined sugar and processed foods, and lowering carbohydrate intake, have been shown to be an excellent alternative to intensive insulin therapy. ...
Type 1 diabetes mellitus is a serious autoimmune disease for which no cure is available. The treatment includes insulin therapy, carbohydrate counting, eating healthy foods, exercising regularly, and maintaining a healthy weight. The goal is to keep blood glucose levels close to normal most of the time to delay or prevent complications. Despite the increase in the use of insulin pumps and continuous glucose monitors in recent years, the management of type 1 diabetes remains suboptimal in terms of glycaemic control and normal glycated haemoglobin (HbA1c) level. This article discusses the case of a child with type 1 diabetes who was successfully treated with a very low-carbohydrate diet, resulting in normal levels of HbA1c and normal blood glucose 95% of the time in a range of 70–180 mg/dL (4.0 mmol/L−10 mmol/L). Therefore, further studies are needed to verify how a very low carbohydrate diet impacts child development.
... In contrast, in an observational study on 11 adult patients with T1D who followed a KD (<55 g of carbohydrates), the KD was associated with good HbA1c levels and reduced glucose variability, but also with dyslipidemia and an increased frequency of hypoglycemic events [94]. In the case report by Toth C. et al. [95], ketogenic paleolithic diet was proposed in a 19-years-old male with newly diagnosed T1DM and resulted in normalization of glucose levels, increased C-peptide levels and increased triglycerides and LDL cholesterol. It is worth to note that in this case report there is no mention about ketone bodies level range; moreover, C-peptide level increase was documented only 2 months after diagnosis, when it is not so uncommon to observe a rise in C-peptide levels (honeymoon phase) [96]. ...
Full-text available
Low-carb and ketogenic diets are popular among clinicians and patients, but the appropriateness of reducing carbohydrates intake in obese patients and in patients with diabetes is still debated. Studies in the literature are indeed controversial, possibly because these diets are generally poorly defined; this, together with the intrinsic complexity of dietary interventions, makes it difficult to compare results from different studies. Despite the evidence that reducing carbohydrates intake lowers body weight and, in patients with type 2 diabetes, improves glucose control, few data are available about sustainability, safety and efficacy in the long-term. In this review we explored the possible role of low-carb and ketogenic diets in the pathogenesis and management of type 2 diabetes and obesity. Furthermore, we also reviewed evidence of carbohydrates restriction in both pathogenesis of type 1 diabetes, through gut microbiota modification, and treatment of type 1 diabetes, addressing the legitimate concerns about the use of such diets in patients who are ketosis-prone and often have not completed their growth.
... Previously we have published a case of soft palate cancer halted by the paleolithic ketogenic diet for 20 months [10]. We also reported successful management of cases of autoimmune conditions including type 1 diabetes [24,25] and cases with epilepsy [26,27] and metabolic syndrome [28] using the paleolithic ketogenic diet. In another case study we reported that a full dietary adherence is needed to halt disease progression in rectal cancer [29]. ...
Full-text available
Background: Ketogenic diets have repeatedly been suggested for the treatment of cancer. To date, only a few case studies reporting long term benefits associated with such diets have been published. Case report: Here we present a case where recurrent cervical intraepithelial neoplasia (CIN), a premalignant condition of cervical cancer, was successfully treated with the paleolithic ketogenic diet. The patient had a history of high grade CIN in 2011, which was successfully treated with cervical conization and fractional curettage. In October 2015 she was found to have a recurrence of high grade CIN (HSIL: High Grade Squamous Intraepithelial Lesion). The patient was then commenced on the paleolithic ketogenic diet and her repeat Pap (Papanicolaou) smear three months later was found to have reverted to normal. The patient has remained on the paleolithic ketogenic diet for 26 months, her repeat smears have stayed normal, and she is free of symptoms and side effects. Conclusion: We conclude that the diet was effective and safe in this patient. As a major benefit the patient was able to avoid a hysterectomy, which is the standard treatment for recurrent high-grade CIN. We believe that the paleolithic ketogenic diet combines benefits of both paleolithic and classical ketogenic diets, while excluding their disadvantages.
Autoimmune diseases are complex conditions that are increasing in incidence worldwide. Autoimmune disorders are often associated clinical challenges in regards to clear diagnoses, comorbidities, and effective disease management and treatment strategies. Importantly, research suggests that an individual’s nutritional status and metabolic health, such as the presence of obesity or metabolic syndrome, may play a role in the risk, pathophysiology, and management of autoimmune diseases. Further, adherence to Western or Mediterranean-style dietary patterns, as well as intake of specific macronutrients (e.g., carbohydrates, protein, fatty acids), micronutrients (e.g., vitamin D, selenium, sodium) and non-nutrient dietary factors (e.g., food contaminants, gut microbiome profiles), may modulate autoimmune disease development and complications. Thus, nutritional interventions may represent an effective approach to mitigate risk and support the management of autoimmune disorders.
Carbohydrate restriction, used since the 1700s to prolong survival in people with diabetes, fell out of favor after the discovery of insulin. Despite costly pharmacological and technological developments in the last few decades, current therapies do not achieve optimal outcomes, and most people with diabetes remain at high risk for micro- and macrovascular complications. Recently, low-carbohydrate diets have regained popularity, with preliminary evidence of benefit for body weight, postprandial hyperglycemia, hyperinsulinemia, and other cardiometabolic risk factors in type 2 diabetes and, with more limited data, in type 1 diabetes. High-quality, long-term trials are needed to assess safety concerns and determine whether this old dietary approach might help people with diabetes attain clinical targets more effectively, and at a lower cost, than conventional treatment.
Objectives: To evaluate glycemic control among children and adults with type 1 diabetes mellitus (T1DM) who consume a very low-carbohydrate diet (VLCD). Methods: We conducted an online survey of an international social media group for people with T1DM who follow a VLCD. Respondents included adults and parents of children with T1DM. We assessed current hemoglobin A1c (HbA1c) (primary measure), change in HbA1c after the self-reported beginning of the VLCD, total daily insulin dose, and adverse events. We obtained confirmatory data from diabetes care providers and medical records. Results: Of 316 respondents, 131 (42%) were parents of children with T1DM, and 57% were of female sex. Suggestive evidence of T1DM (based on a 3-tier scoring system in which researchers took into consideration age and weight at diagnosis, pancreatic autoimmunity, insulin requirement, and clinical presentation) was obtained for 273 (86%) respondents. The mean age at diagnosis was 16 ± 14 years, the duration of diabetes was 11 ± 13 years, and the time following a VLCD was 2.2 ± 3.9 years. Participants had a mean daily carbohydrate intake of 36 ± 15 g. Reported mean HbA1c was 5.67% ± 0.66%. Only 7 (2%) respondents reported diabetes-related hospitalizations in the past year, including 4 (1%) for ketoacidosis and 2 (1%) for hypoglycemia. Conclusions: Exceptional glycemic control of T1DM with low rates of adverse events was reported by a community of children and adults who consume a VLCD. The generalizability of these findings requires further studies, including high-quality randomized controlled trials.
Full-text available
Introduction Childhood absence epilepsy is an epilepsy syndrome responding relatively well to the ketogenic diet with one-third of patients becoming seizure-free. Less restrictive variants of the classical ketogenic diet, however, have been shown to confer similar benefits. Beneficial effects of high fat, low-carbohydrate diets are often explained in evolutionary terms. However, the paleolithic diet itself which advocates a return to the human evolutionary diet has not yet been studied in epilepsy. Results Here, we present a case of a 7-year-old child with absence epilepsy successfully treated with the paleolithic ketogenic diet alone. In addition to seizure freedom achieved within 6 weeks, developmental and behavioral improvements were noted. The child remained seizure-free when subsequently shifted toward a paleolithic diet. Conclusion It is concluded that the paleolithic ketogenic diet was effective, safe and feasible in the treatment of this case of childhood absence epilepsy.
Full-text available
The very-high-fat ketogenic diet can worsen lipid levels in children with pre-existing hyperlipidemia by increasing serum lipoproteins and reducing antiatherogenic high-density lipoproteins. A retrospective chart review of 160 children treated with the ketogenic diet from September 2000 to May 2011 was performed. Twelve children with pre-existing hyperlipidemia were identified. Lipid levels including total cholesterol, low-density lipoprotein, triglycerides, high-density lipoprotein, and total cholesterol/high-density lipoprotein were measured pre-diet and at 3, 6, and 12 months of treatment. During treatment, there was a significant reduction in mean total cholesterol, low-density lipoprotein, and total cholesterol/high-density lipoprotein. Total cholesterol and low-density lipoprotein were normalized in 8 and 7 children at 6 months; and 9 and 9 children at 12 months respectively. At 6 and 12 months, tot cholesterol/HDL ratio was normalized in 5 and 7 children respectively. Diet modifications were made to achieve healthy lipid levels. By extrapolating the data, it suggests lipid levels can be controlled in children and adults with ketogenic diet treatment.
Full-text available
Cow’s milk-based infant formulas and cow’s milk consumption in childhood have been suggested to promote the development of type 1 diabetes mellitus and other immune-mediated or neurological diseases. Epidemiological studies in man have led to the hypothesis that introduction of cow’s milk-based infant formula within the first 3 months of life is associated with increased risk of type 1 diabetes mellitus. Furthermore, in animal models of type 1 diabetes mellitus, cow’s milk proteins have been proven to be ‘diabetogenic’. However, the issue seems far from being resolved. Several epidemiological studies and, more importantly, the first prospective trials did not show an association between early exposure to cow’s milk and type 1 diabetes mellitus. In animal models, cow’s milk proteins are modestly and variably diabetogenic, wheat or soyabean proteins in the diet cause higher rates of autoimmune diabetes. In both man and rodents there is increasing evidence that the gut-associated immune system plays a major role in disease development, probably because of disturbed oral tolerance mechanisms. Oral tolerance depends on immunological homeostasis and normal maturation of the gut. These factors are influenced by growth factors and cytokines from breast milk, normal bacterial colonization, infections and diet. All these factors have been proposed as risk factors for type 1 diabetes mellitus. Hence, cow’s milk proteins may provide mimicry epitopes relevant in autoimmunity, as well as destabilizing oral tolerance mechanisms by biologically active peptides. The concept of dietary regulation of autoimmunity does not apply only to cow’s milk protein, but also to other dietary proteins.
Full-text available
Background Reduction of dietary carbohydrates and corresponding insulin doses stabilizes and lowers mean blood glucose in individuals with type 1 diabetes within days. The long-term adherence for persons who have learned this technique is unknown. To assess adherence over 4 years in such a group the present audit was done retrospectively by record analysis for individuals who have attended an educational course. Adherence was assessed from HbA1c changes and individuals’ own reports. Findings Altogether 48 persons with diabetes duration of 24 ± 12 years and HbA1c > = 6.1% (Mono-S; DCCT = 7.1%) attended the course. Mean HbA1c for all attendees was at start, at 3 months and 4 years 7.6% ± 1.0%, 6.3 ± 0.7%, 6.9 ± 1.0% respectively. The number of non-adherent persons was 25 (52%). HbA1c in this group was at start, at 3 months and 4 years: 7.5 ±1.1%, 6.5 ± 0.8%, 7.4 ± 0.9%. In the group of 23 (48%) adherent persons mean HbA1c was at start, at 3 months and 4 years 7.7 ± 1.0%, 6.4 ± 0.9%, 6.4 ± 0.8%. Conclusion Attending an educational course on dietary carbohydrate reduction and corresponding insulin reduction in type 1 diabetes gave lasting improvement. About half of the individuals adhered to the program after 4 years. The method may be useful in informed and motivated persons with type 1 diabetes. The number needed to treat to have lasting effect in 1 was 2.
Full-text available
To examine persistence of C-peptide production by ultrasensitive assay years after onset of type 1 diabetes and factors associated with preserving β-cell function. Serum C-peptide levels, a marker of insulin production and surviving β-cells, were measured in human subjects (n = 182) by ultrasensitive assay, as was β-cell functioning. Twenty-two times more sensitive than standard assays, this assay's lower detection limit is 1.5 pmol/L. Disease duration, age at onset, age, sex, and autoantibody titers were analyzed by regression analysis to determine their relationship to C-peptide production. Another group of four patients was serially studied for up to 20 weeks to examine C-peptide levels and functioning. The ultrasensitive assay detected C-peptide in 10% of individuals 31-40 years after disease onset and with percentages higher at shorter duration. Levels as low as 2.8 ± 1.1 pmol/L responded to hyperglycemia with increased C-peptide production, indicating residual β-cell functioning. Several other analyses showed that β-cells, whose C-peptide production was formerly undetectable, were capable of functioning. Multivariate analysis found disease duration (β = -2.721; P = 0.005) and level of zinc transporter 8 autoantibodies (β = 0.127; P = 0.015) significantly associated with C-peptide production. Unexpectedly, onset at >40 years of age was associated with low C-peptide production, despite short disease duration. The ultrasensitive assay revealed that C-peptide production persists for decades after disease onset and remains functionally responsive. These findings suggest that patients with advanced disease, whose β-cell function was thought to have long ceased, may benefit from interventions to preserve β-cell function or to prevent complications.
Accumulating evidence suggests that low-carbohydrate, high-fat diets are safe and effective to reduce glycemia in diabetic patients without producing significant cardiovascular risks. Most of these studies have been carried out specifically restricting carbohydrates, which tends to lead to increased protein intake, thus reducing the ketosis. However, diets that limit protein as well as carbohydrates, entailing a composition very high in fat, appear even more effective to reduce glucose and whole-body glucose metabolism in humans. In animal models, low-carbohydrate, high-protein diets do not produce ketosis or reduce glycemia but rather cause obesity. However, limiting both protein and carbohydrates as in a classic ketogenic diet remarkably reduces blood glucose in animal models of type 1 and type 2 diabetes and reverses diabetic nephropathy. Future studies should assess if ketogenic diets would be effective to reverse diabetic complications in humans.
A 5-year and 10-month old boy was diagnosed with classical type 1 diabetes mellitus (T1DM) without celiac disease. He started on a gluten-free diet after 2-3 week without need of insulin treatment. At the initiation of gluten-free diet, HbA1c was 7.8% and was stabilised at 5.8%-6.0% without insulin therapy. Fasting blood glucose was maintained at 4.0-5.0 mmol/l. At 16 months after diagnosis the fasting blood glucose was 4.1 mmol/l and after 20 months he is still without daily insulin therapy. There was no alteration in glutamic acid decarboxylase positivity. The gluten-free diet was safe and without side effects. The authors propose that the gluten-free diet has prolonged remission in this patient with T1DM and that further trials are indicated.
Cow's milk β-casein has been proposed as a candidate trigger of autoimmunity associated with type 1 diabetes. In this study, cellular and humoral immunity against β-casein was compared to that against other major cow's milk proteins in patients with recent onset type 1 diabetes and control subjects. T cell responses were found against α-casein, β-casein, β-lactoglobulin and bovine serum albumin in both patients with type 1 diabetes (stimulation index: 0.2–22.8, n=23) and control subjects (stimulation index: 0.1–18.2, n=22), with no significant differences between groups. Twelve (52%) patients and nine (41%) control subjects had stimulation indices >3 to at least one protein, including 9 (39%) patients and 4 (18%) control subjects against β-casein, all but one of these also having elevated responses to α-casein. The highest responses (stimulation index >9) were against α- and β-casein in some patients and control subjects who had the HLA DR3 allele. Antibody levels against α-casein, β-casein and β-lactoglobulin were low in both patients (n=59) and control subjects (n=52). Nevertheless, significantly higher IgG binding to both α-casein in ELISA (P=0.02) and β-casein using ELISA (P=0.02) and RIA (P=0.04) was observed in patients aged <15 years compared to control subjects of similar age. No relationship was found between cellular and humoral immunity against individual antigens. These data show that immune responses to cow's milk are not limited to patients with diabetes and not solely against β-casein.
Diabetic ketoacidosis (DKA) is a life-threatening condition and a major cause of morbidity and mortality in children with type 1 diabetes mellitus. The deficiency of insulin leads to metabolic decompensation, causing hyperglycemia and ketosis that resolves with the administration of insulin and fluids. However, an induced state of ketosis is the basis for the success of the ketogenic diet (KD), which is an effective therapy for children with intractable epilepsy. We report the case of a 2-year-old girl who presented to the emergency department with 1-week history of decreased activity, polyuria, and decreased oral intake. Her past medical history was remarkable for epilepsy, for which she was started on the KD with a significant improvement. Her laboratory evaluation was compatible with DKA, and fluids and insulin were given until correction. Because of concerns regarding recurrence of her seizures, the KD was resumed along with the simultaneous use of insulin glargine and insulin aspart. Urine ketones were kept in the moderate range to keep the effect of ketosis on seizure control. Under this combined therapy, the patient remained seizure-free with no new episodes of DKA.
Dietary cholesterol comes exclusively from animal sources, thus it is naturally present in our diet and tissues. It is an important component of cell membranes and a precursor of bile acids, steroid hormones and vitamin D. Contrary to phytosterols (originated from plants), cholesterol is synthesised in the human body in order to maintain a stable pool when dietary intake is low. Given the necessity for cholesterol, very effective intestinal uptake mechanisms and enterohepatic bile acid and cholesterol reabsorption cycles exist; conversely, phytosterols are poorly absorbed and, indeed, rapidly excreted. Dietary cholesterol content does not significantly influence plasma cholesterol values, which are regulated by different genetic and nutritional factors that influence cholesterol absorption or synthesis. Some subjects are hyper-absorbers and others are hyper-responders, which implies new therapeutic issues. Epidemiological data do not support a link between dietary cholesterol and CVD. Recent biological data concerning the effect of dietary cholesterol on LDL receptor-related protein may explain the complexity of the effect of cholesterol on CVD risk.