Side-effects of Ketosis
 

Everything in life has side-effects. Some are good and some are bad. Sometimes it is the lesser of two evils that we must choose. High carbohydrate diets have side-effects such as heart disease, diabetes, aging, hyperinsulinemia, raised cholesterol and weight gain. Everything we put into our body from water to drugs to food has side-effects. In the case of water, they are generally good side-effects.

Now before anyone freaks out about what I’m about to post, remember where the above side-effects of a pattern of high carbohydrate intake has taken you. And if you have ever taken Fen-Phen or Meridia or Fastin or Ephedra or caffeine or anything else to lose weight, you should consider the side-effects of those drugs and chemicals as worse than the side-effects of ketosis.

Remember that all this information is due to my diligence in wanting to know what is going on in my body during a low-carbohydrate ketogenic diet. I’m the type who reads all the side-effects on all drug medications I’ve taken in my life and who reads the fine print on medical documents that I sign. Most people would be too frightened to take any drug or have any surgical operation performed on them if they did this. So if you are that type of person, forget reading this. Know that most research has shown and I quote: “Most adverse effects were mild, self-limited, and occurred early.”

Now for those who want to know the worst and best and how to mitigate side-effects, read on.

To make this easy reading I’m going to list what I’ve learned so far and then present the data. As I learn more, I’ll update this post.

There haven’t been a lot of studies done on the effects of ketogenic diets for weight loss, but there have been plenty of studies regarding ketogenic diets for control of epilepsy. Some of these studies were done on non-epileptic rats and mice. Rats and mice are exceptionally good research animals due to the fact that their endocrine system is very similar to humans. Some side-effects come from smaller studies where percentages may be exaggerated or symptoms may be due to other sources such as medications taken concurrently. Some studies were done on children so the effects may have been increased.


EFFECTS OF KETOSIS
Ketosis creates a measurable amount of acetone in the mouth. (Remedial measure: brush teeth and mouth with baking soda, increase water intake, eat vegetables)

Ketosis decreases aspartate in the brain, but glutamate and glutamine remain unchanged with increase in glutamate conversion to GABA. (GABA controls nerve cells in brain from firing too fast. Same effect as when taking Valium). Utilization of neutral amino acids to increase glutamine.

3. 10% will have trouble reaching ketosis
4. 21% will have an intolerance of the rapid onset of ketosis
5. 41% will become constipated (Remedial measure: increase fiber intake)
6. 47% will experience hypoglycaemia (symptoms: fatigue, weakness, confusion, dizziness, irritability, a rapid heartbeat, anxiety, sweating, trembling, hunger, and headaches i.e. withdrawal symptoms from sugar addiction.)
7. 16% will refuse to drink fluids (which are critical to deter acid build-up during ketosis)
8. 16% will experience lack of appetite (this is good if you are on a weight loss diet)
9. 26% will have nausea and vomiting
10. 65% will have a rise in total serum cholesterol (although HDL will increase proportionally)
11. 32% will have periods of anorexia (aversion to food)
12. 9% will have symptomatic metabolic acidosis when associated with infection
13. 9% will have carnitine insufficiency during early part of ketogenic diet (supplement with L-Carnitine)
14. 8% will have high levels of uric acid in the urine (Drink water, eat vegetables, neutralize with bases)

Remember if these things above are the worse that can happen to you on a ketogenic diet that is tons better than heart disease, high LDL, diabetes, etc. SO DON'T FREAK OUT. Take supplements, drink plenty of water, and EAT YOUR VEGETABLES!

Some definitions are included at end of abstracts
-------------------------------

J Neurosci Res 2001 Dec 1;66(5):931-40

Ketogenic diet, amino acid metabolism, and seizure control.

Yudkoff M, Daikhin Y, Nissim I, Lazarow A, Nissim I.

Division of Child Development and Rehabilitation, Children's Hospital of Philadelphia, 34th St. and Civic Center Blvd., Philadelphia, PA 19104, USA. yudkoff~email.chop.edu

The ketogenic diet has been utilized for many years as an adjunctive therapy in the management of epilepsy, especially in those children for whom antiepileptic drugs have not permitted complete relief. The biochemical basis of the dietary effect is unclear. One possibility is that the diet leads to alterations in the metabolism of brain amino acids, most importantly glutamic acid, the major excitatory neurotransmitter. In this review, we explore the theme. We present evidence that ketosis can lead to the following: 1) a diminution in the rate of glutamate transamination to aspartate that occurs because of reduced availability of oxaloacetate, the ketoacid precursor to aspartate; 2) enhanced conversion of glutamate to GABA; and 3) increased uptake of neutral amino acids into the brain. Transport of these compounds involves an uptake system that exchanges the neutral amino acid for glutamine. The result is increased release from the brain of glutamate, particularly glutamate that had been resident in the synaptic space, in the form of glutamine. These putative adaptations of amino acid metabolism occur as the system evolves from a glucose-based fuel economy to one that utilizes ketone bodies as metabolic substrates. We consider mechanisms by which such changes might lead to the antiepileptic effect. Copyright 2001 Wiley-Liss, Inc.

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J Neurosci Res 2001 Oct 15;66(2):272-81
Brain amino acid metabolism and ketosis.

Yudkoff M, Daikhin Y, Nissim I, Lazarow A, Nissim I.

Division of Child Development and Rehabilitation, Children's Hospital of Philadelphia, 34th Street and Civic Center Boulevard, Philadelphia, PA 19104, USA. yudkoff~email.chop.edu

The relationship between ketosis and brain amino acid metabolism was studied in mice that consumed a ketogenic diet (>90% of calories as lipid). After 3 days on the diet the blood concentration of 3-OH-butyrate was approximately 5 mmol/l (control = 0.06-0.1 mmol/l). In forebrain and cerebellum the concentration of 3-OH-butyrate was approximately 10-fold higher than control. Brain [citrate] and [lactate] were greater in the ketotic animals. The concentration of whole brain free coenzyme A was lower in ketotic mice. Brain [aspartate] was reduced in forebrain and cerebellum, but [glutamate] and [glutamine] were unchanged. When [(15)N]leucine was administered to follow N metabolism, this labeled amino acid accumulated to a greater extent in the blood and brain of ketotic mice. Total brain aspartate ((14)N + (15)N) was reduced in the ketotic group. The [(15)N]aspartate/[(15)N]glutamate ratio was lower in ketotic animals, consistent with a shift in the equilibrium of the aspartate aminotransferase reaction away from aspartate. Label in [(15)N]GABA and total [(15)N]GABA was increased in ketotic animals. When the ketotic animals were injected with glucose, there was a partial blunting of ketoacidemia within 40 min as well as an increase of brain [aspartate], which was similar to control. When [U-(13)C(6)]glucose was injected, the (13)C label appeared rapidly in brain lactate and in amino acids. Label in brain [U-(13)C(3)]lactate was greater in the ketotic group. The ratio of brain (13)C-amino acid/(13)C-lactate, which reflects the fraction of amino acid carbon that is derived from glucose, was much lower in ketosis, indicating that another carbon source, i.e., ketone bodies, were precursor to aspartate, glutamate, glutamine and GABA. Copyright 2001 Wiley-Liss, Inc.
---------------------------------------------

Rev Neurol 2001 Nov 16-30;33(10):909-15
[Complications of treatment of epilepsy by a ketogenic diet]

[Article in Spanish]

Rios VG.

Saniago del Estero 2475, Santa Fe, 3000, Argentina.

INTRODUCTION: It was originally claimed that the ketogenic diet (KC) caused no major adverse effects. Few studies have been done to analyze the side effects and complications of the KC. OBJECTIVES: To analyze the side effects and complications seen in a group of patients on KC compared with those described in the international literature. PATIENTS AND METHODS: We made a prospective evaluation of 22 patients aged between one and nineteen years, over an average period of 25 months. All had some type of refractory epilepsy and had been included in a group treated following classical KC guidelines. RESULTS: The side effects and complications during admission were delay in onset of the ketotic state (10.5%), intolerance of the rapid onset of ketosis (21%), hypoglycaemia (47.37%), refusal to drink fluids (15.79%), lack of appetite (15.79%), and nausea and vomiting (26.31%). During treatment the serum cholesterol rose in 64.7% of the children, 40.91% were constipated, 31.82% had periods of anorexia, symptomatic metabolic acidosis occurred during intercurrent infections in 9.09%, renal calculi in 9.09%, carnitine insufficiency in 9.09% and severe complications which led to hospital admission in 21.05%. CONCLUSIONS: Our group of patients had no more side effects or complications than those described in the literature. KC may lead to complications, especially when strict guidelines for control and follow up are not used. However, they are usually easy to correct if detected early.------------------------------------------

Pediatr Neurol 2002 Apr;26(4):288-92

The ketogenic diet: a review of the experience at Connecticut Children's Medical Center.

DiMario FJ, Holland J.

Department of Pediatrics, University of Connecticut School of Medicine, Division of Pediatric Neurology at Connecticut Children's Medical Center, 06106, Hartford, CT, USA

We undertook a retrospective analysis of epilepsy patients referred and treated for more than 6 months with the ketogenic diet during 1994-1999 at Connecticut Children's Medical Center. Outcome measures included antiepileptic drug number, seizure frequency, electroencephalogram background/paroxysmal activity, and adverse effects at 6 months and 1 year on the ketogenic diet. The final cohort included 24 of 48 referred patients (mean age, 6.5 years; range = 1-15 years of age). The etiology of epilepsy was equally divided between idiopathic and cryptogenic epilepsy and symptomatic epilepsy. Intention to treat analysis revealed that 35% (17 of 48) achieved more than 50% reduction in seizure frequency, and 8.5% (four of 48) were seizure-free by 6 months. A sustained 50% or greater reduction at 1 year was observed in 23% (11 of 48), and the same 8.5% (four of 48) remained seizure-free. None of these improvements were statistically related to age (P = 0.97), sex (P = 0.78), or epilepsy etiology (P = 0.80). The number of antiepileptic drugs used per patient decreased. Electroencephalogram at 1 year demonstrated an improvement in background in 31% (five of 16 patients) and a reduction in paroxysmal features in 37.5% (6 of 16 patients). Most adverse effects were mild, self-limited, and occurred early. Hyperuricemia (more than 6 mg/dL) was more persistent in three patients.

PMID: 11992756 [PubMed - in process]

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Epilepsy Res 2002 Feb;48(3):221-7
The ketogenic diet in children, adolescents and young adults with refractory epilepsy: an Italian multicentric experience.

Coppola G, Veggiotti P, Cusmai R, Bertoli S, Cardinali S, Dionisi-Vici C, Elia M, Lispi ML, Sarnelli C, Tagliabue A, Toraldo C, Pascotto A.

Clinic of Child Neuropsychiatry, Second University of Naples, Via Pansini 5, 80131, Naples, Italy

Purpose: This collaborative study by three Italian groups of child neuropsychiatrists was carried on to evaluate the efficacy and safety of the classic 4:1 ketogenic diet as add-on treatment in refractory partial or generalized epilepsy in children, adolescents and young adults. Methods: We performed a prospective add-on study in 56 refractory epilepsy young patients (age 1-23 years, mean 10.4 years), all with both symptomatic and cryptogenic, generalized or partial epilepsies. Child neuropsychiatrists worked with nutritional team for sample selection and patients management. The ketogenic diet was added to the baseline antiepileptic drugs and the efficacy was rated according to seizure type and frequency. During treatment, seizure frequency, side effects, urine and blood ketone levels and other parameters were systematically evaluated. Results: Patients have been treated for 1-18 months (mean 5 months). A >50% reduction in seizure frequency was gained in 37.5 and 26.8% of patients after 3 and 6 months, respectively, at 12 months, this number fell by 8.9%. No significant relationship between diet efficacy and seizure or epilepsy type, age at diet onset, sex and etiology of epilepsy was noted. Nevertheless, it seems noteworthy that 64% of our patients with neuronal migration disorders improved on this diet. Adverse effects occurred, mainly in the first weeks of treatment, in 32 patients (57.1%), but were generally mild and transient. In seven patients (12.5%) it was possible to withdraw one to two AED after 3-4 months on ketogenic diet. Conclusion: This initial experience with the ketogenic diet was effective in difficult-to-treat patients with partial and generalized epilepsies, though its efficacy dropped significantly by 9-12 months.

PMID: 11904241 [PubMed - in process]

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Epilepsia
Volume 42 Issue 11 Page 1445 - November 2001

Carnitine Levels and the Ketogenic Diet
*Elizabeth Berry-Kravis, *Gayle Booth, *Ana Carolina Sanchez, and *Jean Woodbury-Kolb
Purpose: To determine the long-term effect of the ketogenic diet (KD) on carnitine levels and whether carnitine depletion is a significant cause of clinical complications during KD initiation or treatment.
Methods: Carnitine levels at 0, 1, 6, 12, and 24 months of diet treatment, carnitine antiepileptic drug (AED) history, lowest blood glucose and time to achieve ketosis during diet initiation, and diet complications were analyzed for 38 consecutive patients who initiated the KD from May 1997 to March 2000. Carnitine levels at follow-up were analyzed for eight patients started on the diet before to May 1997.
Results: Total carnitine (TC) at diet initiation correlated negatively with the number of AEDs at diet initiation but not with number of past AEDs, lowest blood glucose, or time to ketosis. TC decreased in the first months of diet treatment and then stabilized or increased slightly with long term treatment. Only 19 of patients were supplemented with carnitine for low TC. No patient showed clinical signs of carnitine deficiency.
Conclusions: Multiple AED exposure lowers TC, but actual TC deficiency in patients initiating the KD is not common, and TC levels do not appear to predict hypoglycemia or problems achieving ketosis. Mild carnitine depletion may occur early in KD treatment and occasionally TC decreases out of the normal range, without clinical symptoms. TC stabilizes or increases back toward baseline with long-term treatment, and most patients do not require carnitine supplementation.
aspartate
<amino acid> A nonessential amino acid that plays a critical part of the enzyme in the liver that transfers nitrogen-containing amino groups, either in building new proteins and amino acids or in breaking down proteins and amino acids for energy and detoxifying the nitrogen in the form of urea.
Depleted levels of aspartic acid may occur temporarily within certain tissues under stress, but, because the body is able to make its own aspartic acid to replace any depletion, deficiency states do not occur.
Aspartic acid is abundant in plants, especially in sprouting seeds. In protein, it exists mainly in the form of its amide, asparagine.
The popular sweetener Aspartame is a combination of aspartic acid and phenylalanine. Aspartic acid is considered nontoxic.
GABA
gamma aminobutyric acid
<biochemistry> An important amino acid which functions as the most prevalent inhibitory neurotransmitter in the central nervous system.
Gamma aminobutyric acid works in partnership with a derivative of Vitamin B-6, pyridoxine, to cross from the axons to the dendrites through the synaptic cleft, in response to an electrical signal in the neuron and inhibits message transmission. This helps control the nerve cells from firing too fast, which would overload the system.
The action of gamma aminobutyric acid decreases epileptic seizures and muscle spasms by inhibiting electrical signals in this manner. Studies have shown that the site of action in the brain of benzodiazepams, including Valium, is directly coupled to the brain receptor for gamma aminobutyric acid.

Acetone
(Ketone, Dimethyl)

Toxicity
Toxicity Data (Remember acetone levels never get this high during a ketogic diet)
· UNR-MAN LDLO: 1159 mg/kg
Target Organs:
· Brain and Coverings (Recordings from specific areas of cns)
· Sense Organs (Other olfaction effects)
· Sense Organs (Conjunctiva irritation)
· Behavioral (General anesthetic)
· Behavioral (Muscle weakness)
· Behavioral (Muscle contraction or spasticity)
· Lungs, Thorax or Respiration (Respiratory depression)
· Lungs, Thorax or Respiration (Other changes)
· Kidney, Ureter, or Bladder (Renal function tests depressed)
· Fertility (Post-implantation mortality)
Only selected entries shown here.
Effects:
· Inhalation: irritating to mucous membranes and upper respiratory tract.
Synonyms
Acetone (german, dutch, polish)
Chevron Acetone
Dimethylformaldehyde
Dimethylketal
Dimethyl Ketone
Ketone Propane
Beta-ketopropane
2-Propanone
Pyroacetic Acid
Pyroacetic Ether
CAS # 67-64-1
Incompatibles
Bases
Oxidizing Agents
Reducing Agents
Structure
Formula: C3H6O

Also, I might add that the ketogenic diet for epilepsy appears to create a much higher ketotic state than Atkin's or any other ketogenic weight loss plan. From what I have read so far the diet consists of 91% fat and 9% protein, but I will have to verify. In other words, the symptoms and side-effects described above are drastically reduced in people in a lower ketotic state where urinary ketones are in the trace to moderate range.

Classic ketogenic diet used for these studies
 

The traditional 4:1 (four parts fat : one part carbohydrate, one part protein) classical ketogenic diet and 41% used the medium chain triglyceride diet (60% MCT fat).

In other words, in the above studies the diet was 66% fat, 17% carbohydrate and 17% protein which is more carbohydrate than Atkin's induction.

A type of fat called medium chain triglycerides appear to stimulate ketosis.

As always Voyeur very interesting read and food for thought...

Bonnie

Another side-effect
 

Thanks, Bonnie

Correction on classic 4:1 ketogenic diet. It is 80% fat and 20% combined protein and carbs. It is often supplemented with MCT (i.e. coconut oil).

Here is another piece of information on ketogenic diets. The very best way to prevent the following side-effect is by drinking lots of water.

Pediatr Nephrol 2000 Nov;15(1-2):125-8

Risk factors for urolithiasis in children on the ketogenic diet.

Furth SL, Casey JC, Pyzik PL, Neu AM, Docimo SG, Vining EP, Freeman JM, Fivush BA.

Kidney stones have been associated with use of the ketogenic diet in children with refractory seizure disorders. We performed a case-control study examining risk factors for the development of stones on the ketogenic diet, and prospectively followed children initiating the ketogenic diet to evaluate the incidence of urolithiasis. Clinical characteristics of 18 children presenting with stones (8 uric acid stones, 6 mixed calcium/uric acid stones, 1 calcium oxalate/phosphate stone, 3 stones not evaluated) were compared with characteristics of non-stone-forming children initiating the ketogenic diet at Johns Hopkins since July 1996. Since July 1996, 112 children initiating the ketogenic diet have been followed for development of stones. Follow-up times on the diet range from 2 months to 2.5 years. Of 112 children, 6 have developed stones (3 uric acid, 3 mixed calcium/uric acid stones) (0.8 children developing stones/ 100 patient-months at risk). Comparisons of children presenting with stones on the ketogenic diet with characteristics of the entire cohort initiating the ketogenic diet suggest younger age at diet initiation and hypercalciuria are risk factors for the development of stones. Prospective evaluation of children initiating the ketogenic diet revealed that almost 40% of patients had elevated fasting urine calcium: creatinine ratios at baseline; this increased to 75% after 6 months on the diet. Median urine pH was 5.5 at diet initiation, and remained at 6.0 thereafter. In a subset of patients tested, urinary citrate excretion fell from a mean of 252 mg/24 h pre diet initiation to 52 mg/24 h while on the diet. Uric acid excretion remained normal. Patients maintained on the ketogenic diet often have evidence of hypercalciuria, acid urine, and low urinary citrate excretion. In conjunction with low fluid intake, these patients are at high risk for both uric acid and calcium stone formation.

What Is a Kidney Stone?

Kidney stones are non-life-threatening, however, they can be painful.

A kidney stone develops from crystals that separate from urine and build up on the inner surfaces of the kidney. Normally, urine contains chemicals that prevent or inhibit the crystals from forming. These inhibitors do not seem to work for everyone, however, and some people form stones. If the crystals remain tiny enough, they will travel through the urinary tract and pass out of the body in the urine without even being noticed.

Kidney stones may contain various combinations of chemicals. The most common type of stone contains calcium in combination with either oxalate or phosphate. These chemicals are part of a person's normal diet and make up important parts of the body, such as bones and muscles.

A less common type of stone is caused by infection in the urinary tract. This type of stone is called a struvite or infection stone. Much less common are the uric acid stone and the rare cystine stone.

Urolithiasis is the medical term used to describe stones occurring in the urinary tract. Other frequently used terms are urinary tract stone disease and nephrolithiasis. Doctors also use terms that describe the location of the stone in the urinary tract. For example, a ureteral stone (or ureterolithiasis) is a kidney stone found in the ureter. To keep things simple, the term "kidney stones" is used throughout this e-text document.

Gallstones and kidney stones are not related. They form in different areas of the body. If a person has a gallstone, he or she is not likely to develop kidney stones.

Absorptive hypercalciuria occurs when the body absorbs too much calcium and empties the extra calcium into the urine. This high level of calcium in the urine causes crystals of calcium oxalate or calcium phosphate to form in the kidneys or urinary tract.

Other causes of kidney stones are hyperuricosuria (a disorder of uric acid metabolism), gout, excess intake of vitamin D, and blockage of the urinary tact. Certain diuretics (water pills) or calcium-based antacids may increase the risk of forming kidney stones by increasing the amount of calcium in the urine.

Calcium oxalate stones may also form in people who have a chronic inflammation of the bowel or who have had an intestinal bypass operation, or ostomy surgery. As mentioned above, struvite stones can form in people who have had a urinary tract infection.

A patient may be asked to collect his or her urine for 24 hours after a stone has passed or been removed. The sample is used to measure urine volume and levels of acidity, calcium, sodium, uric acid, oxalate, citrate, and creatinine (a byproduct of protein metabolism). The doctor will use this information to determine the cause of the stone.

Calcium and Kidney Stone

Although patients with calcium stones have been encouraged to restrict calcium intake in the past, studies are now strongly indicating that dietary calcium is actually protective against many cases of calcium oxalate stones. Large studies of both men and women found that those with the highest intake of dietary calcium had a much lower risk for stones than those who had little calcium in their diets. Some experts believe that dietary calcium may help by binding the oxalate in foods, preventing it from being absorbed into the blood and excreted into the urine. In one study of women, however, those who took calcium supplements, had a 20% higher risk. Some experts speculate that this higher risk may occur because supplements are usually taken in the morning either without food or with breakfast, which is typically low in oxalates. Taking supplements with later meals may not incur the same risk. It should also be noted that many people with calcium stones have reduced bone density from resorption (the breakdown of bone that releases calcium into the blood stream). Limiting calcium intake in such people could actually promote further bone loss. Some calcium stone patients who have supersaturation of calcium in the urine and who are not at risk for bone loss may need to restrict calcium, but more studies are needed to define this group precisely.

UROLITHIASIS (Kidney Stones)

Canadians appear to have a very high incident of kidney stones and the occurence is particularly high in Newfoundland (11, 12). In U.S., South Carolina has the highest urolithiasis rate. South Carolina also has the highest U.S. rate for cardivascular deaths (10). Both Newfoundland and South Carolina regions have "very soft" drinking waters with little magnesium (11).

In Canada, calcium urolithiasis accounts for 70 to 80% of the total kidney-stone problems (12). In the U.S., about 67% of all kidney stones are composed of calcium oxalate or calcium hydroxyapatite (11).

Several researchers have used the magnesium/calcium ratio as an index of susceptibility of urine to form kidney-stones in patients (10,13,14). In general, patients with a urinary magnesium/calcium ratio of 0.7 is normal, whereas a value lower than 0.7 may be considered as stone-forming. The ratio is especially low in the Canadian "Kidney Stone Patients", indicating inadequate magnesium intake.

The oral magnesium supplementation has proven very effective in the prevention of kidney-stone formation (14).

The traditional ratio is 2 mg of calcium for every 1 mg of magnesium.

Okay, we finally have a study on Atkins diet so I can put the actual side-effects from doing Atkins for six-months. (The study is continuing, but these are the symptoms of six-months only. There may be other side-effects down the road.) But so far, so good.

The American Journal of Medicine
Volume 113, Issue 1, July 2002, Pages 30-36

Effect of 6-month adherence to a very low carbohydrate diet program*1

Eric C. Westman MD, MHS, , a, b, William S. Yancy MDa, b, Joel S. Edman DScc, Keith F. Tomlina and Christine E. Perkins MSWa

Quote from study:

Adverse effects
At some point during the 24 weeks, 28 subjects (68%) reported constipation, 26 (63%) reported bad breath, 21 (51%) reported headache, 4 (10%) noted hair loss, and 1 woman (3%) reported increased menstrual bleeding. One subject reported an episode of orthostatic hypotension soon after restarting the diet after a period of nonadherence. This subject continued the diet program with no further similar episodes. Another subject had moderately severe headaches daily for 3 months, which resolved without treatment. Thirty-five subjects (85%) reported more energy, 11 (27%) had decreased heartburn, 30 (73%) had fewer cravings for sweets, 21 (51%) had improved mood, and 8 women (26%) had fewer premenstrual symptoms and less menstrual cramping.

I'm curious as to why they lumped these side effects with the adverse ones. Was 'positive effects' too much for them to swallow?

Nat

Doctors do not know why ketosis stops siezures in epileptics. One study theorized that it was the increase in GABA in the brain. This study says it is the acetone.


Med Sci Monit 2002 Aug;8(8):HY19-24

Ketogenic diet: does acetone stop seizures?

Likhodii S, Burnham M.

Department of Pharmacology and Bloorview Epilepsy Research Program, Faculty of Medicine, University of Toronto, Toronto, Canada.

BACKGROUND: The mechanism of action of the ketogenic diet, a therapy for refractory epilepsy, is unknown. Our hypothesis is that acetone, one of three ketones elevated by the ketogenic diet, is directly responsible for the diet's anticonvulsant effects. This study examined the basic concepts of this hypothesis. MATERIAL/METHODS: Rats were acutely injected with acetone intraperitoneally at doses of 1 or 10 mmol/kg, or received acetone chronically in drinking water (1% v/v) for 10 days before being injected with a 1 mmol/kg dose of acetone. Controls consumed regular water and were injected with vehicle. A pentylenetetrazole seizure test was administered 15 min after the injections. Following the test, acetone was measured in the cerebrospinal fluid. RESULTS: A 10 mmol/kg injection of acetone suppressed seizures in 60% of rats (P<0.05). A chronic administration of acetone followed by a 1 mmol/kg injection suppressed seizures in 47% of rats (P<0.05). The acetone concentrations in these rats were 10.3I2.3 and 1.0I0.2 mmol/L, respectively. The effect of the acute 1 mmol/kg injection (without acetone pretreatment) was not statistically significant. This dose elevated acetone to 1.1I0.1 mmol/L in the cerebrospinal fluid. CONCLUSIONS: Our findings suggest that acetone is an anticonvulsant and that chronic administration may enhance its action. Linking acetone to the effects of the ketogenic diet requires further research. In particular, it will be important to confirm that the ketogenic diet generates relevant concentrations of acetone.

Interesting. Out of the 14 "side effects" listed in the initial post, I've had 0. The one and only adverse effect I've had is intermittent, benign muscle twitches. Magnesium has helped(300mg/day-supplemented, +seeds/nuts), but only about half. I eat a good deal of Calcium as well, so am a bit bewildered.

With the MCT's, are there recommendations as to supplement these as well?

You know, I haven't had any of the side effects either that I can tell. My doctor was all for any low carb plan, but really insisted on lots of water and veggies to keep the kidney stones away.

However, a wellness nurse at my husband's work was really against it and because I don't defend the WOL anymore I just changed the subject. She was shocked however when my total cholesterol was only 166.

I think it comes natural for the medical community to be negative first. They are scientists.

Shelleoy

The only adverse side effect I had was constipation. And now that I have been low-carbing for over 6 months, my body has adjusted and I don't need added fibre at all.

Also, I have had all of the positive side effects, except for the menstrual ones and the jury is still out on that one.

;-Deb

Kidney Stones
 

I am considering the Adkins diet. It might surprise you that my heart doctor said, "Go for it." and my family doctor the same, but I have read several things that concern me since I seem to develop a kidney stone almost every year. What advice do you have.

Ron

Ron,

It is important to find out what kind of kidney stones you are getting to determine the cause:

"A patient may be asked to collect his or her urine for 24 hours after a stone has passed or been removed. The sample is used to measure urine volume and levels of acidity, calcium, sodium, uric acid, oxalate, citrate, and creatinine (a byproduct of protein metabolism). The doctor will use this information to determine the cause of the stone."

Have you been watching your calcium/magnesium intake? This is important. Also, water intake is important. What are you doing already for your problem?

Kidney Stones
 

I believe the Drs. report said that the stone was "consistant with calcium oxalate." I am probably about 50-60 oz. of water/diet drinks. I am taking Bovine Colstrum, Renaplex (a Thorne Research product), IP-6 and Inositol as well as 140 mg of magnesium and 150 mg of Calcium plus a broad range of vitamins from Thorne Research.

I forgot to mention that I am taking the IP-6 and Renaplex specifically with the hopes of helping to prevent stones. That is a very recent addition to my supplements. Ron.

I forgot to mention that I am taking the IP-6 and Renaplex specifically with the hopes of helping to prevent stones. That is a very recent addition to my supplements. Ron.

Although there is actually no proof that adults on Atkins or any kind of a ketogenic diet develop kidney stones, there is evidence that less than 5% of children on a ketogenic diet for up to two years may develop kidney stones. Of the ones that do develop stones, they are primarily of the uric acid type. The problem with children is that they are not conscientious enough to drink enough water.

If you continue to drink about a gallon of water per day (you'll be thirstier on Atkins) and get your calcium from cheese in the Atkins diet, you should do well. Studies have shown that getting most of your calcium from your diet instead of from supplements will reduce risk of stones. Of course, with someone who has had stones before, there is no guarantee that they won't have stones again, no matter what diet they are on. Also, you should be taking your calcium supplements in the evening and up your magnesium to 400 mg. This advice is per Dr. Eades in Protein Power (another low-carb diet doctor).

Increasing magnesium is important because calcium is not absorbed by the body without the presence of magnesium. And excess calcium will therefore be flushed out in the urine which causes hypercalciuria leading to the type of stones you have had (calcium oxalate).

I haven't heard much about the other supplements that you are taking, but vitamins are normally helpful.

With this program, your risk of kidney stones will probably not be increased and the benefits of the Atkins Diet will greatly outweigh any possible side-effects. You'll be glad you did.

Will following the neanderthin plan lead to a risk of kidney stones? I don't feel its right to drink too much water, sorry i never feel like drinking too much and it just means i goto the toilet a little too much. I drink the following, do i need to alter what i do to reduce risk:

morning 7-9 : 250ml water, 500 ml coffee.
11-12: 250ml green tea, 250ml water
2-3: 250ml water, 250ml green tea
5-6: 250ml mint tea, somtimes 250 ml water
8-10: 250ml water, 250ml camomile tea.
total: 2750 ml
varies between 2250 and 2750ml
Thanks (i don't eat cheese, occasionally take calcium supplement , though neanderthin says you don't need to)

Voyajer--

There seem to be differences among low-carb diet authorities on whether ketosis is even a necessary state to aim for. I've read that Atkins himself puts less emphasis on it. Schwarzbein counsels against it. What's your view?

Sheldon

Actually, both questions about enough water and ketosis are related.

As far as ketosis being safe let me quote from Gary Taubes New York Times article "What if it's all been a big fat lie?":



Okay, but the question was should we aim for ketosis. The truth is that there are always some level of ketone bodies in our blood. They can't be measured with the ketostix. They increase after vigorous exercise. They are natural.

But the other truth is that the very high states of ketosis where the ketostix turn purple do have the highest diuretic effect. This means your body loses more electrolytes. This is why your thirst increases. This is why everyone on Atkins should be taking potassium and keeping hydrated.

But here's the catch: according to the Westman study on the Atkins diet, the heavier the ketosis that the person was in, the more weight he lost. So the higher the ketotic state, the more weight loss, but the higher chance of kidney stones due to the diuretic effect. Of course, this study was done on the induction phase only. The induction phase lasted for six months in this study and no one developed kidney stones being in heavy ketosis for six months. However, induction has never been tested for longer than six months. Most people in the Atkins induction phase do not reach purple on the ketostix anyway and generally move on to OWL where they add carbs. I would say all this information shows that heavy ketosis is safe for six months and depending on the individual may be the best method of weight loss. That is to say, if a person has resistance to weight loss and is very overweight, this may be the best plan.

AND this is where the water issue comes in. The less in ketosis you are, the less water you need. Dr. Lutz low-carb diet "Life Without Bread" calls for 72 g carb per day. He says don't drink any more water than you feel the need to drink. He says you are unlikely to reach ketosis on this amount of carbs.

Neanderthin incorporates a high amount of fruit. Most people are unlikely to be in deep ketosis eating the amount of carbs in fruit. However, anyone taking calcium should also be taking magnesium. Magnesium prevents stone formation.

Protein Power Lifeplan allows for 35 g carb daily which maintains a less heavy ketotic state. He still recommends high water intake and potassium.

Usually, the more g of carb you eat even on different low-carb diets makes you crave carbs more. The more grams of carb you eat means you have to watch calories a little closer too.

It's a matter of personal choice.

One caveat
 

Hi, Voyager. I would like to make one caveat to your quotes. You said The problem with this is they are talking about the most weight in a certain amount of time.

I am planning to reduce my weight by about 110 pounds total. On TSP, I am expecting it to take me 2 to 3 years. But I will be able to attain my goal.

It bothers me that they keep putting it that way, that you can only lose a lot of weight if you go extreme. It's not true. It only matters if you expect to be able to lose it faster.

;-Deb

Deb,

Thanks for adding that point. Your point is right on the money. This isn't a race to see who loses weight fastest. This is about a lifestyle change.

For some people Atkin's induction is too restrictive and anyway it really isn't meant to be a lifelong way of eating. You need to go through the phases. Whatever low-carb way of eating is the one that a person can maintain for a lifetime, that's the one they should be on.

It will do no good to lose weight fast only to go off the diet and gain it back.

Every low-carb diet has its good points and it depends on the individual's ability to adhere to the way of eating that matters. Slow and steady wins the race. You only lose the battle if you quit trying.

Voyajer
Thanks for all your research efforts. I was interested in more details about 21% are intolerant of the rapid onset of ketosis . Is intolerance just discomfort and is there anyway to overcome the intolerance?

I have tried to do induction over and over ( and lose a few pounds everytime), but end up quitting because of the tremendous water loss, huge thirst and heart palpitations, I guess from the electrolyte imbalance irritating a minor heart problem.

Also, my dr. suggested the zone diet and all the symptoms immediately disappeared and I feel fantastic. But is eating 100carbs a day lowcarb? It is described as putting your body on a fat burning pathway, can that be true while eating so many carbs?

Voyager,

Thank heaven - another research hound!

I had a few questions related to your first post in this thread, from 2002, if you've got a moment.

>9% will have carnitine insufficiency during early part of ketogenic diet (supplement with L-Carnitine)

This is interesting, as L-Carnitine (which is not exactly an amino acid but is grouped with them) is found mainly in meats. www.googlism.com (a little quick-study google alternative I love that gives you just the gist of a topic typed in) notes that:

-l-carnitine is needed to release energy from fat

Here's a great description of why L-carnitine helps with low-carbing so much, and why it's depleted early on in ketosis:
"Carnitine helps transport fatty acids across the mitochondrial membrane thereby increasing fatty acid oxidation. Since the membrane is somewhat impermeable to long-chain fatty acids they must be shuttled into the mitochondria. Carnitine with acyl CoA is converted to acyl carnitine by carnitine acyltransferase I. Translocase brings the acyl carnitine into the mitochondria, the acyl carnitines are converted back into acyl CoA, oxidized and energy is released. Carnitine may also transport acetyl groups back to the cytoplasm for fatty acid synthesis. In addition carnitine stimulates acetoacetate oxidation. Acetoacetate and D-3-hydroxybutyrate are ketone bodies that are formed from acetyl CoA, a product of fatty acid oxidation. Diabetes and fasting increase the use of oxaloacetate to form glucose. If oxaloacetate is in short supply acetyl CoA does not enter the citric acid cycle but is diverted to form acetoacetate. Acetoacetate and D-3-hydroxybutyrate are sources of energy and are preferred by the heart and adrenal cortex over glucose. While the brain uses glucose as its major source of fuel, during starvation it adapts to utilize acetoacetate. High levels of acetoacetate in the blood indicate an abundance of acetyl units and in turn lead to a decrease in the rate of lipolysis in fat tissue. Carnitine stimulates an increase in acetoacetate oxidation which in turn decreases serum acetoacetate, thereby increasing lipolysis of fat."

Ta-da... I'm very happy to have found that (at www.nutritionfocus.com).

Would love to hear any further thought on the topic that you (or anyone else) has.

>14. 8% will have high levels of uric acid in the urine (Drink water, eat vegetables, neutralize with bases)

First, do you know where all these percentages actually came from? (Just curious.) Second, what exactly do you mean by neutralize with bases? Eat in an alkaline manner... vegetatively, so to speak? And do you recall the reason that the uric acid is produced? (You may have mentioned it in that first post, I'll go back and re-read it.)

One additional question about aspartate, which you mentioned. (Anti-aspartame issues aside for the moment...) ... do you glean from your reading that having asparagine or aspartate is very important particularly in low-carbing, and if one does indeed get aspartate via the aspartame in Diet sodas, no need to think about supplements? On the other hand, is there any reason why aparagine/aspartate in any realistic quantity would be COUNTERproductive to low-carbing?

Thanks.

CBCB

I read something today that suggested that citric acid, not aspartame, was the real culprit behind the stalls that are often associated with Nutrasweet (the brand name of aspartame). Citric acid - which adds a sour flavor and a preservative effect - often joins sugar and artificial sweeteners in sodas, candy, and other sweet-tart treats. I think I remember that it also appears in the sugar metabolism (Krebs) cycle at some point.

Sorry for the incompleteness/sketchy nature of this post - it is late; I'm tired; I don't have the link handy - but you research hounds might want to follow this scent.

Just a suggestion. See you good folks in the morning -

Gotbeer

GotBeer, thanks for bringing that up... if anyone knows how citric acid intake actually would or could stall fat-burning, would love to hear the mechanism... I've looked at diagrams of the citric acid cycle, but never saw how citric acid itself fit into the picture.

Diet Dr. Pepper is one diet soda that does not have citric acid in it.. they have a caffeine-free version too but of course it has aspartame in it. Now, Diet Rite cola is a caffeine-free, aspartame-free diet cola, but it's got citric acid. Sigh.

thanks!
 

Voyager,

Thank god - another research hound! It is for people like you that make me visit this site. Thanks a lot. I'll keep coming.

Voyager, I'm sure you have read about pH stuff. Meat/protein
are acidic food.. for sure my urea nitrogen has gone up a little but in range , urine pH moved from 7 to 6 ...

does the body get depleted of mineral buffer to keep things in
neutral range.. I'm confused a bit. Share your research if you have found any .. anybody here.

thanks
neeam

uric acid kidney stones and vitamin C
 

Hi folks - I'm a newbie here, so I apologize if I missed this point -
I had a history of uric acid kidney stones, getting them more or less annually for 4 years BEFORE going on a low-carb diet (usually following some dehydration event). I also had occasional sharp pains in my left knee that I attributed to an old war wound, but my dad said sounded like his gout.

When I went on the diet, my MD was concerned and wanted me to get my blood chemistry checked. It was fine, except that my uric acid was high. He wanted to put me on Allopurinol. I did my research, and discovered three things that relate to this:
1) Tea causes a false positive on the uric acid test. I drink 1-2 pots of tea daily, so I knew I had to stop that and retake the test.
2) Some foods, including cold-water fish like salmon and sardines, are high in purines and lead to high uric acid. I was having a tin of sardines most afternoons. So I stopped.
3) An old study (that I no longer have the reference for) said Vitamin C promotes the excretion of uric acid.

So I stopped the tea, stopped the sardines, and took 2500mg C every day. I took the test again in two weeks and my uric acid was back to normal.

I have continued taking vitamin C ever since. Three weeks ago I went completely off the diet to enjoy New England apple season uninhibited, and to catch up on the few foods I'd been missing. I have gained a few pounds, but more significant...I stopped the vitamin C, and my knee pain came back. I immediately took 3500mg, and the pain promptly faded.

It is not proof, but I am guessing that Vitamin C does indeed help with the uric acid kidney stone problem.

I don't know if I'm posting right but can someone tell me whet the 3 #'s after stats:
Does it corespond to start weight/current weight/goal weight?
If so......Bonnie....hats off and holy crap!!

I am one of the ketosis casualties, I'm afraid. Although I lost ~35 lbs on Atkins, and enjoyed eating the food the entire time, at a certain point my weight loss slowed down to a crawl and was no longer a reward commensurate with the side effects of the keto diet.

This is because I am one of those people who gets horrible headaches from ketosis. Some peoples' systems are ultra-sensitve to ketones, and mine seems to be one of them. The deeper the ketosis, the worse the headache--and no amount of painkiller will get rid of it. This effect persists regardless of the amount of water I drink. It only goes away completely when I get over 100 carbs/day, which can hardly be called a low carb diet.