I have had insomnia for close to two decades and amazingly, very few things helped as much as a keto diet. At first, I thought this was odd but later I read about many other people who had better sleep while on KETO. Also, I read somewhwere -may be on Lyle's board- that KETO diets slow down the metabolism via reduction in T3 and T4 secretion and this is one of the reasons they help you preserve muscle mass. So is this true? Do they actually decrease T3 and T4 levels? If not, what is the better sleep attributable to?
Sub7
|
-
07-29-2005, 11:23 AM #1
Do Ketogenic Diets Slow Metabolism?
-
07-29-2005, 12:54 PM #2
I don't think keto diets slow metabolism any more than other diets, and probably less, since it preserves muscle better, which works to keep up the metabolism.
I've also found I sleep better in keto, and wake constantly when I'm doing a carb-up. I think it's just the effect of the insulin spikes and dips that wake me up when I eat carbs, rather than something special about keto.65% fat, 30% protein, 5% carbs = keto.
http://www.eileengormley.com/ Funny science fiction for bodybuilders
-
07-29-2005, 01:22 PM #3
Eileen, you might be interested in this: beneficial effect of keto diet on the sleep disorder narcolepsy has been reported in the medical literature:
---
Husain AM, et al. Diet therapy for narcolepsy. Neurology, 22 June 2004; 62 (12): 2300-2302
Abstract—
The effects of a low-carbohydrate, ketogenic diet (LCKD) on sleepiness and other narcolepsy symptoms were studied. Nine patients with narcolepsy were asked to adhere to the Atkins’ diet plan, and their symptoms were assessed using the Narcolepsy Symptom Status Questionnaire (NSSQ). The NSSQ–Total score decreased by 18% from 161.9 to 133.5 (p = 0.0019) over 8 weeks. Patients with narcolepsy experienced modest improvements in daytime sleepiness on an LCKD.
Narcolepsy is a syndrome characterized by excessive daytime sleepiness (EDS), cataplexy, sleep paralysis, and hypnagogic hallucinations. However, despite optimal pharmacologic management, daytime sleepiness persists in many patients. The effect of diet on the sleep–wake cycle in narcolepsy has not been studied in detail. We examined the effect of a low-carbohydrate, ketogenic diet (LCKD) on daytime sleepiness in patients with narcolepsy already on optimal doses of stimulant medications.
Methods.
Patients were recruited from the narcolepsy clinic at the Veterans Affairs Medical Center, Durham, NC. Inclusion criteria consisted of a diagnosis of narcolepsy with continued daytime sleepiness despite optimal stimulant therapy. Narcolepsy was defined as the presence of EDS with either unequivocal cataplexy or presence of at least two sleep-onset REM periods on a Multiple Sleep Latency Test (MSLT). 1 Additionally, patients had to have a body mass index (BMI) of at least 20 kg/m2 and agree to modify their diet per instructions. Patients were excluded if they were pregnant or nursing or had a serious medical condition.
Diet instructions for the LCKD were derived from a popular lay press book, Dr. Atkins’ New Diet Revolution. 2 Patients were instructed to restrict carbohydrate intake to <20 g/day. They were advised to take a standard multivitamin and drink copious fluids daily. Follow-up group visits occurred every other week for 8 weeks. Patients were instructed not to change their stimulant medication dosage.
Sleepiness was measured at baseline and weeks 2, 4, and 8 using three validated self-administered scales: the Narcolepsy Symptoms Severity Questionnaire (NSSQ), the Epworth Sleepiness Scale (ESS), and the Stanford Sleepiness Scale (SSS). 3,4 Adherence to the diet intervention was measured by self-report and urinary ketones. Patients self-monitored urine ketone levels with dipsticks at the same time daily using the following semiquantitative scale: 0 = none, 1 = trace (up to 5 mg/dL), 2 = small (5 to 40 mg/dL), 3 = moderate (40 to 80 mg/dL), 4 = large-80 (80 to 160 mg/dL), 5 = large-160 (>160 mg/dL). The mean level of urine ketones for each week was calculated for each patient. Weight and vital signs were measured at each visit. A fasting lipid profile and routine serum chemistries were obtained at baseline and study termination.
Linear mixed-effects models, with a random intercept and time (i.e., week) as a fixed effect, were used to analyze the effect of the diet on sleepiness symptoms as measured by the NSSQ, ESS, and SSS. Paired t-tests, or Wilcoxon signed-rank tests where appropriate, were used to compare baseline to week 8 vital and laboratory measurements for the eight participants who completed the study. A p value of <=0.05 was considered significant. Analyses were performed using SAS Statistical Software (version 8.02; SAS Institute, Cary, NC).
Results.
Nine patients were recruited for the study. The mean ± SD age was 47.6 ± 10.9 years; eight were men, seven were African American, two were Caucasian. The mean body weight at baseline was 100.9 ± 19.8 kg, and the mean BMI was 32.8 ± 6.9 kg/m2. One subject dropped out after 4 weeks owing to inability to adhere to the diet.
Significant improvements were seen on the NSSQ–Total score and the following subscales: Sleepiness, Sleep Attacks, and Sleep Paralysis (table;figure 1). The Total score on the NSSQ decreased by 18% from 161.9 at baseline to 133.5 at week 8 (p = 0.0019). In addition, the Sleepiness Subscale score decreased by 22% from 51.0 to 39.6 (p = 0.017), the Sleep Attacks Subscale score decreased by 13% from 46.0 to 40.0 (p = 0.016), and the Sleep Paralysis Subscale score decreased by 24% from 21.1 to 16.0 (p = 0.015). The ESS and SSS did not change significantly over the 8-week duration of the study.
Graphic
Table Predicted scores* on sleep questionnaires
Graphic
Figure 1. Predicted mean scores of Narcolepsy Symptom Status Questionnaire (NSSQ) subscales by linear mixed-effects model. Diamonds = Sleepiness; squares = Sleep Attacks; triangles = Cataplexy; x’s = Sleep Paralysis; circles = Vivid Dreams.
The mean number of days since the previous visit that participants were not adherent to the diet increased from 0.3 ± 0.5 day at week 2 to 1.3 ± 1.3 days at week 8. The mean urine ketone levels by self-testing increased from 0 at baseline to 2.8 ± 0.6 at week 1, peaked at 3.7 ± 0.9 at week 2, and declined gradually to a plateau at 2.8 ± 1.1 at week 8 (figure 2). Over the 8 weeks, body weight decreased from 99.3 ± 20.7 kg at baseline to 92.2 ± 19.8 kg (p < 0.0001). No adverse changes were noted in blood pressure, serum lipid profiles, or serum chemistry tests.
Graphic
Figure 2. Mean (SE) urine ketone levels for each week (n = 9 for weeks 0 to 4, n = 8 for weeks 5 to 8). Urine ketone scale: 0 = none, 1 = trace (up to 5 mg/dL), 2 = small (5 to 40 mg/dL), 3 = moderate (40 to 80 mg/dL), 4 = large-80 (80 to 160 mg/dL); 5 = large-160 (>160 mg/dL).
There were no serious adverse events reported during this study. Four patients (44%) had transient side effects (headache, leg cramps, irritability, and difficulty with concentration); however, none was severe enough to prompt discontinuation of the study or the diet. No patient reported a worsening of daytime sleepiness.
Discussion.
EDS is often debilitating for patients with narcolepsy. Many patients continue to experience daytime sleepiness despite the optimal use of stimulant medications. Another treatment commonly recommended to narcolepsy patients is dietary modification, even though its effect has not been studied prospectively.
In the current study, dietary modification resulted in significant improvements of narcolepsy symptoms as measured by the NSSQ. The NSSQ–Total score decreased by 18% after 8 weeks of treatment, whereas the Sleepiness Subscale score decreased by 22%, Sleep Attacks Subscale by 13%, and Sleep Paralysis Subscale by 24%.
Serum ketones are one potential mechanism for the observed effect on narcolepsy symptoms, although the pathway involved has not been identified. Urinary ketones were highest in the first 2 weeks and then decreased somewhat to plateau at week 8. A similar pattern of ketonuria with this diet has been noted previously. 5 The most likely reason for the gradual decline in urine ketones is that subjects increased their carbohydrate intake. Alternatively, it is possible that the body adjusts physiologically to reduced carbohydrate intake.
Another intriguing mechanism to consider involves the role of orexin (hypocretin). Patients with narcolepsy have been shown to have impaired orexin signaling. 6 Hypoglycemia tends to activate orexin-containing neurons. 7 It is possible that the LCKD, by inducing relative hypoglycemia (blood glucose lower than baseline), increases the activation of orexin-containing neurons, which in turn improves daytime sleepiness.
Dietary effects on sleep and fatigue have been evaluated in other situations. In one study, volunteers without a sleep disorder who consumed a high-carbohydrate, low-fat diet spent less time in slow wave sleep than those who consumed either a balanced or a low-carbohydrate, high-fat diet. 8 In a review of occupational sleep and fatigue, the authors noted that simple carbohydrates produce a transient increase in alertness, followed by a decrease in alertness after a few hours. 9 These studies support the view that diet influences sleep and that carbohydrates may exacerbate sleepiness in certain individuals.
One possible limitation of this study was the method used to measure daytime sleepiness. The gold standard for measuring the degree of daytime sleepiness is the MSLT. This test was not employed for this study because of the considerable cost and time required for its use. It can be argued that daytime alertness may have improved because of decreases in body weight. As this variable was not controlled in this study, it remains a possibility, although benefits were noted by patients early in the study before substantial weight loss occurred. Though this study suggests that dietary therapy may improve daytime sleepiness, a randomized trial with a comparison intervention is needed to determine if weight loss or other factors contributed to the observed improvements in sleepiness symptoms.
-
07-29-2005, 02:35 PM #4
-
-
07-29-2005, 03:17 PM #5
I have also experianced better sleep. I also fall asleep much faster. It used to take me atleast 45-60 min. to fall asleep. Now I usually fall asleep soon after my head hits the pillow. I feel that is why I have so much energy on this diet, I am getting better rest.
6.24.05-210Lbs
7.1.05-208Lbs
7.7.05-205Lbs
7.21.05-202Lbs
7.28.05-199Lbs :)
8.13.05-198Lbs
8.22.05-197Lbs
-
07-29-2005, 07:13 PM #6
-
07-29-2005, 08:44 PM #7
-
07-30-2005, 08:40 PM #8
-
-
07-30-2005, 10:16 PM #9
- Join Date: Sep 2004
- Location: Schenectady, New York, United States
- Age: 43
- Posts: 11,914
- Rep Power: 4072
Keto does change a lot of things for people.
IE, I do not sleep so well on keto, but I have MUCH more energy and strength, but less cardiovascular endurance. It's kind of funny how changing the way you eat can have such a gigantic impact on your life as a whole.I've gained and lost over 100lbs more times than any man alive should. Do as I say and not as I do.
-
07-31-2005, 11:15 PM #10Originally Posted by skelooth
I also notice that i've got less cariovascular endurance and i don't understand why, I was thinking that lipid was the fuel for endurance training when glycogene is completly used....
-
08-01-2005, 11:22 AM #11
Fat can supply enough energry to fuel activities up to 65-70% intensity. After that, you've got a shortfall, which generally needs carbs. So walking, moderate cycling, jogging, sports with natural breaks like tennis etc, are all fine with a purely keto diet. Even moderate lifting works since you've got rests between sets. But once you go past that 70% threshold, you'll notice life getting a lot harder. Most people on CKD go for short duration cardio like HIIT rather than going for long runs.
People who do a lot of endurance cardio often find that they need to do TKD, or even stick to a carb-based diet.65% fat, 30% protein, 5% carbs = keto.
http://www.eileengormley.com/ Funny science fiction for bodybuilders
-
08-02-2005, 03:19 PM #12
Bookmarks