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  #1   ^
Old Sun, Jun-09-02, 11:39
Voyajer's Avatar
Voyajer Voyajer is offline
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Default 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.

----------------------------------------

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]

-------------------------------------------------


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]

-----------------------------------------------------

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
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  #2   ^
Old Sun, Jun-09-02, 13:32
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Voyajer Voyajer is offline
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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.
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Old Mon, Jun-10-02, 16:10
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Voyajer Voyajer is offline
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Default 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.
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Old Mon, Jun-10-02, 17:20
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Bonnie Bonnie is offline
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As always Voyeur very interesting read and food for thought...

Bonnie
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Old Thu, Jun-13-02, 08:24
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Voyajer Voyajer is offline
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Default 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.
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Old Fri, Jul-19-02, 15:00
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Voyajer Voyajer is offline
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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.
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Old Fri, Jul-19-02, 15:09
Natrushka Natrushka is offline
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Quote:
Originally posted by Voyajer
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
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Old Thu, Aug-15-02, 20:33
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Voyajer Voyajer is offline
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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.
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Old Fri, Aug-16-02, 12:20
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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?
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  #10   ^
Old Fri, Aug-16-02, 13:38
cre8tivgrl's Avatar
cre8tivgrl cre8tivgrl is offline
Senior Member
Posts: 2,045
 
Plan: Low carb
Stats: 20/08/00 Female 5'10"
BF:not/low/enough
Progress: 60%
Location: The great Northwest
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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
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  #11   ^
Old Sat, Aug-17-02, 10:06
DebPenny's Avatar
DebPenny DebPenny is offline
Senior Member
Posts: 1,514
 
Plan: TSP/PPLP/low-cal/My own
Stats: 250/209/150 Female 63.5 inches
BF:
Progress: 41%
Location: Sacramento, CA
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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
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  #12   ^
Old Mon, Aug-26-02, 17:38
yohe yohe is offline
New Member
Posts: 4
 
Plan: Adkins
Stats: 255/255/180
BF:
Progress: 0%
Question 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
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  #13   ^
Old Mon, Aug-26-02, 17:52
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Voyajer Voyajer is offline
Senior Member
Posts: 475
 
Plan: Protein Power LP Dilletan
Stats: 164/145/138 Female 5'7"
BF:
Progress: 73%
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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?
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Old Mon, Aug-26-02, 18:53
yohe yohe is offline
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Posts: 4
 
Plan: Adkins
Stats: 255/255/180
BF:
Progress: 0%
Question 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.
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  #15   ^
Old Mon, Aug-26-02, 18:55
yohe yohe is offline
New Member
Posts: 4
 
Plan: Adkins
Stats: 255/255/180
BF:
Progress: 0%
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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.
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