Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study

Cardiovasc Diabetol. 2009; 8: 35.

Published online 2009 July 16. doi:  10.1186/1475-2840-8-35

PMCID: PMC2724493

Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study

Tommy Jönsson,1 Yvonne Granfeldt,2 Bo Ahrén,1 Ulla-Carin Branell,3 Gunvor Pålsson,2 Anita Hansson,2 Margareta Söderström,4 and Staffan Lindeberg1

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Abstract

Background

Our aim was to compare the effects of a Paleolithic ('Old Stone Age') diet and a diabetes diet as generally recommended on risk factors for cardiovascular disease in patients with type 2 diabetes not treated with insulin.

Methods

In a randomized cross-over study, 13 patients with type 2 diabetes, 3 women and 10 men, were instructed to eat a Paleolithic diet based on lean meat, fish, fruits, vegetables, root vegetables, eggs and nuts; and a Diabetes diet designed in accordance with dietary guidelines during two consecutive 3-month periods. Outcome variables included changes in weight, waist circumference, serum lipids, C-reactive protein, blood pressure, glycated haemoglobin (HbA1c), and areas under the curve for plasma glucose and plasma insulin in the 75 g oral glucose tolerance test. Dietary intake was evaluated by use of 4-day weighed food records.

Results

Study participants had on average a diabetes duration of 9 years, a mean HbA1c of 6,6% units by Mono-S standard and were usually treated with metformin alone (3 subjects) or metformin in combination with a sulfonylurea (3 subjects) or a thiazolidinedione (3 subjects). Mean average dose of metformin was 1031 mg per day. Compared to the diabetes diet, the Paleolithic diet resulted in lower mean values of HbA1c (-0.4% units, p = 0.01), triacylglycerol (-0.4 mmol/L, p = 0.003), diastolic blood pressure (-4 mmHg, p = 0.03), weight (-3 kg, p = 0.01), BMI (-1 kg/m2, p = 0.04) and waist circumference (-4 cm, p = 0.02), and higher mean values of high density lipoprotein cholesterol (+0.08 mmol/L, p = 0.03). The Paleolithic diet was mainly lower in cereals and dairy products, and higher in fruits, vegetables, meat and eggs, as compared with the Diabetes diet. Further, the Paleolithic diet was lower in total energy, energy density, carbohydrate, dietary glycemic load, saturated fatty acids and calcium, and higher in unsaturated fatty acids, dietary cholesterol and several vitamins. Dietary GI was slightly lower in the Paleolithic diet (GI = 50) than in the Diabetic diet (GI = 55).

Conclusion

Over a 3-month study period, a Paleolithic diet improved glycemic control and several cardiovascular risk factors compared to a Diabetes diet in patients with type 2 diabetes.

Trial registration

ClinicalTrials.gov NCT00435240.

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Background

While dietary management is a cornerstone in the treatment of type 2 diabetes, high quality data on the efficacy of dietary treatment of type 2 diabetes are lacking, according to a recent Cochrane review [1]. Since nutritional science is hampered by confounders, an evolutionary approach has been suggested. It has been postulated that foods that were regularly eaten during human evolution, in particular during the Paleolithic (the 'Old Stone Age', 2.5–0.01 million years BP), may be optimal for prevention and treatment of type 2 diabetes, CVD and insulin resistance [2,3]. A Paleolithic diet is a modern dietary regimen based on foods presumably eaten regularly during the Paleolithic, which includes lean meat, fish, shellfish, fruits, vegetables, roots, eggs and nuts, but not grains, dairy products, salt or refined fats and sugar, which became staple foods long after the appearance of fully modern humans.

To date, only a few studies have examined the effects of a Paleolithic diet on disease and risk factors for disease. In a randomized controlled study in 29 men with ischemic heart disease (IHD) and impaired glucose tolerance or type 2 diabetes (mean HbA1C 4.8% at baseline), we found improved glucose tolerance independent of weight-loss after 12 weeks of Paleolithic diet compared to a Mediterranean-like diet [4]. In the same study, the Paleolithic diet was reportedly lower in glycemic load (GL) than the Mediterranean-like diet [4]. The clinical relevance of glycemic index (GI) and GL is presently being discussed [5]. Some studies show beneficial effects of a low GI/GL diet on risk factors for CVD in diabetes, while other studies do not [6-8]. In a non-controlled study on 14 healthy individuals, Österdahl et al found that three weeks on a Paleolithic diet significantly reduced weight, BMI, waist circumference, systolic blood pressure (SBP) and plasminogen activator inhibitor-1 (PAI-1) [9]. In another non-controlled study in nine healthy overweight individuals where intervention food was supplied and weight kept steady, Frassetto et al found that ten days of a Paleolithic diet improved diastolic blood pressure (DBP), glucose tolerance, insulin sensitivity and lipid profiles [10]. In a randomized controlled feeding trial in domestic swine, we found higher insulin sensitivity, lower C-reactive protein (CRP) and lower DBP after 15 months of a Paleolithic diet, compared with a cereal-based swine feed [11]. This study also showed a low-grade inflammation of the pancreas in the swine who had eaten a cereal based swine feed [11]. In a non-controlled study of ten Australian Aborigines with diabetes and a mean BMI of 27 kg/m2, O'Dea found that reversion to a hunter-gatherer lifestyle during 7 weeks led to 10% weight loss and reductions in fasting and 2 hour glucose and fasting insulin [12]. In a similar study on healthy Australian Aborigines by the same authors, the insulin response to 70 g of starch from white bread was reduced, while the glucose response was not, after 10–12 weeks of reversion to a traditional lifestyle [13]. In an epidemiologic study, we found that traditional Pacific Islanders of Kitava, Papua New Guinea, had no signs of IHD, stroke or markers of the metabolic syndrome, possibly because of their traditional lifestyle [14-16]. Thus, we have previously shown beneficial effects from Paleolithic diet on glycemic control and risk markers for CVD in patients with IHD and in domestic pigs. No study, however, has so far examined the same potential beneficial effect of Paleolithic diet when compared to diabetes diet in subjects with type 2 diabetes.

In the present study, therefore, our aim was to examine the effect on glycemic control and risk factors for CVD of food-based (as opposed to macronutrient based) dietary advice according to this Paleolithic diet model over a 3-month period in patients with type 2 diabetes. The patients were recruited in a primary health care setting, and effects of a Paleolithic diet was compared with effects of dietary advice in accordance with current guidelines for people with diabetes [17].

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Methods

Patients

Approval of the study was obtained from the regional Medical Ethics Committee and the trial was registered at ClinicalTrials.gov (Identifier: NCT00435240). The study was a randomized, cross-over, dietary intervention study in 13 patients with type 2 diabetes without insulin treatment, 3 women and 10 men, recruited from three primary health care units in the Lund area in Sweden. We included adult patients with type 2 diabetes and a C-peptide value above zero, unaltered medical diabetes treatment and stable weight since three months before start of study, HbA1c above 5.5% by Mono-S standard, creatinine below130 μmol/L, liver enzymes below four times their respective upper reference value, no chronic oral or injection steroid treatment and no acute coronary event or change in medication of beta blockers or thyroxin since six months before start of study. Exclusion criteria during ongoing study were change in beta blocker or thyroxin medication, chronic oral or injection steroid treatment, warfarin treatment, creatinine above 130 μmol/L or liver enzymes above four times their respective upper reference value, acute coronary event, and physical or psychological illness or changes in personal circumstances which would make further study participation impossible.

Recruitment for the study during routine clinical work was performed by TJ, UCB, GP, AH and MS. In addition, a letter containing written study information was sent by TJ to subjects at two of the health stations who from journal data seemed to match the inclusion criteria. All recruited subjects were given oral and written study information prior to signing a consent form to participate in the study and were then further assessed for eligibility.

Procedure

All eligible subjects were informed of the intention to compare two healthy diets in the treatment of type 2 diabetes and that it was unknown if any of them would be superior to the other. At study start all eligible subjects were randomized to start with either a Diabetes diet in accordance with current guidelines [17] or a Paleolithic diet. Randomization was performed by UCB, GP and AH by opening opaque, sealed envelopes (prepared by TJ) containing a note of the initial diet with equal proportions of envelopes for both diets. After randomization, there was no blinding of dietary assignment to study participants, nor to those administering the interventions or assessing the outcomes. Immediately after randomization, all subjects received oral and written information individually (by UCB, GP or AH) in the morning about their respective initial diet. After three months all subjects switched diets and received new oral and written information individually (by UCB, GP or AH) about the diet of the following three months. Written information with dietary advice and food recipes were similarly formulated for both diets. For increased conformity, the dietary advice and data collection procedure were discussed by all authors except YG at several meetings prior to start of study. Advice about regular physical activity was given equally to all subjects.

The information on the Diabetes diet stated that it should aim at evenly distributed meals with increased intake of vegetables, root vegetables, dietary fiber, whole-grain bread and other whole-grain cereal products, fruits and berries, and decreased intake of total fat with more unsaturated fat. The majority of dietary energy should come from carbohydrates from foods naturally rich in carbohydrate and dietary fiber. The concepts of glycemic index and varied meals through meal planning by the Plate Model were explained [18]. Salt intake was recommended to be kept below 6 g per day.

The information on the Paleolithic diet stated that it should be based on lean meat, fish, fruit, leafy and cruciferous vegetables, root vegetables, eggs and nuts, while excluding dairy products, cereal grains, beans, refined fats, sugar, candy, soft drinks, beer and extra addition of salt. The following items were recommended in limited amounts for the Paleolithic diet: eggs (≤2 per day), nuts (preferentially walnuts), dried fruit, potatoes (≤1 medium-sized per day), rapeseed or olive oil (≤1 tablespoon per day), wine (≤1 glass per day). The intake of other foods was not restricted and no advice was given with regard to proportions of food categories (e.g. animal versus plant foods). The evolutionary rationale for a Paleolithic diet and potential benefits were explained [19].

Evaluation

An oral glucose tolerance test (OGTT) was performed in the morning after obtaining venous blood samples and measurements of blood pressure, weight and waist circumference in the primary care unit (by UCB, GP or AH) at study start, after 3 months (when switching to a new diet) and at the end of the study (after 6 months). 75 g glucose was ingested. Blood samples for plasma glucose and insulin during OGTT were obtained at 0, 15, 30, 60, 90 and 120 minutes. Changes in the area under the curve (AUC) between 0 and 120 min during OGTT for plasma glucose (AUC Glucose0–120) and plasma insulin (AUC Insulin0–120) were predefined primary endpoints, along with changes in body weight, waist circumference, serum lipids, CRP, blood pressure and glycated haemoglobin A1c (HbA1c) by Mono-S standard. The base of the AUC was set at 0 mmol/L for glucose and 0 pmol/L for insulin. The stimulated secretion was represented by the areas under the glucose and insulin curves using levels at 0 min as the base of the area. The Homeostatic model assessment (HOMA) was used for assessing beta-cell function (%B) and insulin sensitivity (%S), as percentages of a normal reference population, and insulin resistance (IR, the reciprocal of %S (100/%S)) [20]. Values for %B, %S, and IR were derived from fasting plasma glucose and insulin using the HOMA2 computer model v2.2 [20]. Insulin sensitivity index (ISI0,120) was calculated from fasting (0 min) and 120 min (post-OGTT) insulin and glucose concentrations [21]. A 4-day weighed food record on four consecutive days, including one weekend day, with weighing of each food item on a digital weighing scale (that could be set to zero), was completed by the participants, starting 6 weeks after initiating each diet. Nutrient compositions were calculated by YG using data from The Swedish Food Database of the National Food Administration in Sweden. GL and GI for the two diets were calculated. Underlying concept of dietary GL and dietary GI is food GI, introduced by Jenkins et al [22], reflecting the postprandial glucose response after a specific food rich in carbohydrate, expressing the quality of the carbohydrates. Wolever and Jenkins also suggested the possibility of ranking diets based on dietary GI calculated from the proportional GI contribution of the included foods containing carbohydrate [23]. To include also the quantity of carbohydrates consumed GL was introduced by Salmerón et al expressing the glycemic effect of the diet [24]. While dietary GI is expressing the quality of the carbohydrates consumed GL represent both the quantity and the quality of the carbohydrates consumed. Thus, dietary GL in this study was calculated as the result from multiplying available carbohydrate (g) for the food reported by the subjects during the 4-day weighed food record with the specific food's GI divided by 100. Available carbohydrate was based on total carbohydrate minus dietary fibre. Food's GI values (glucose as reference) were taken from the compilation by Foster-Powel et al [25]. Dietary GI was calculated as 100 multiplied with dietary GL divided by the amount of available carbohydrate (g) in the diet.

Statistics

A pre-study power calculation showed that 15 subjects would be required to detect, with 80% power and at a significance level of 5%, a 15% reduction in AUC Glucose0–120. Two-way paired t-test was used to analyze within-subject changes in absolute values, while two-way unpaired t-test was used to analyze between-subject changes in absolute values. All outcome variables showed reasonable normal distribution in normal plots. Within-subject changes in outcome variables after first and second diet and within-subject changes in reported dietary intake during first and second diet were used to check for period effects [26]. Mean values of outcome variables and reported dietary intakes for the group starting with Paleolithic diet was compared with the group starting with Diabetes diet in order to check for carry-over effects [26]. Exploratory analyses were performed on outcome variables with significant effects from the Paleolithic diet as compared to the Diabetes diet. Exploratory analyses consisted of bivariate correlations between within-subject differences (Δ) in outcome and dietary variables. Significantly correlating variables were entered into a stepwise forward linear regression analyses.

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Results

Recruitment and participant flow

The study started in January 2005 and the last participant was followed up in September 2007 after which the study was stopped. Out of 26 subjects assessed for eligibility, nine were not eligible since they did not meet the inclusion criteria or refused to participate. Out of the remaining 17 eligible subjects, who were all randomized and started on the study, four subjects were excluded for the following reasons: one starting with Paleolithic diet was wrongly included with ongoing warfarin treatment, one starting with Paleolithic diet was unwilling to continue due to abdominal pains and bloating, one starting with Diabetes diet was excluded after developing leukemia, and one starting with Diabetes diet was excluded after developing heart failure. All reported analyses are "per protocol" analyses on the 13 participants who completed the trial.

Medication

Study participants were on average treated with just above four drugs per day, which usually included metformin alone (3 subjects) or metformin in combination with a sulfonylurea (3 subjects) or a thiazolidinedione (3 subjects)(Table

subjects)(Table1,

1,

,2).

2). Medication usually also included a lipid lowering drug (8 of 13 study participants and always statin treatment) and more than one anti-hypertensive drug per day (Table

(Table1,

1,

,2).

2). All medication remained unchanged during the whole study with the following exceptions:

Table 1 Baseline characteristics (mean ± SD)

Table 2 Baseline differences and carry-over effects between groups with different starting diets (mean ± SD)

One participant stopped taking sulfonylurea (glibencklamide 87.5 mg daily) the day after starting the study with the Paleolithic diet, and was thus on a low dose sulfonylurea at baseline, but without sulfonylurea during both the Paleolithic and Diabetes diet. Exclusion of this participant would not negate any significant effects from the Paleolithic diet compared to the Diabetes diet, but would negate the effect from the Paleolithic diet compared to baseline on systolic blood pressure, and the effect from the Diabetes diet compared to baseline on BMI. Due to concerns for rising blood sugar levels one participant switched hypertensive treatment from a thiazide diuretic to a beta blocker for seven weeks during the Paleolithic diet. Exclusion of this participant would not negate the significant effect on HbA1c, but would negate the effect on diastolic blood pressure. Due to concerns about muscle ache one participant was without lipid-lowering drug treatment for four weeks during the Paleolithic diet. Exclusion of this participant would not negate the significant effects on TG and HDL, but would instead cause also total cholesterol to be significantly lower following the Paleolithic diet compared to the Diabetes diet (p = 0.03). One participant was put on finasteride (5 mg daily, a drug versus benign prostate hyperplasia) during the Paleolithic diet and continued this medication during the following Diabetes diet.

Baseline data

The group starting with the Paleolithic diet differed at baseline only with regard to fasting plasma glucose and AUC glucose being lower and HOMA2 %B being higher compared to the group starting with a Diabetes diet (Table

(Table2).

2). There was no difference between starting groups before or at the end of the study in inclusion/exclusion variables.

Outcome variables

Compared to the Diabetes diet, the Paleolithic diet resulted in lower mean values of HbA1c, TG, DBP, weight, BMI and waist circumference, while mean values for HDL were higher (Table

(Table3,

3, Figure

Figure1).

1). The larger decrease of fasting plasma glucose following the Paleolithic diet nearly reached significance, and SBP also tended to decrease more following the Paleolithic diet. Compared to baseline, the Paleolithic diet lowered mean values of HbA1c, TG, SBP, weight, BMI, waist circumference, fasting plasma glucose, fasting plasma insulin, AUC glucose, ISI0,120, HOMA2 %S and HOMA2 %IR (Table

(Table3).

3). Compared to baseline, the Diabetes diet lowered mean values of BMI, waist circumference and HOMA2 %S (Table

(Table3).

3). Period effects were seen in AUC insulin0–120, AUC insulin0–120 stimulated secretion and HOMA2 %B (Table

(Table4).

4). Carry over effects were seen in HbA1c (Table

(Table2,

2, Figure

Figure1

1).

Table 3

Risk factors for cardiovascular disease after Paleolithic diet and Diabetes diet (mean ± SD, Confidence Interval 95%)

Table 4

Period effects on cardiovascular risk factors after 3 and 6 months in all 13 subjects combined (mean ± SD)

Figure 1

Cardiovascular risk factors with significant effects from Paleolithic diet compared to Diabetes diet. Closed circles depicts individuals starting with Diabetes diet first and open circles depicts individuals starting with Paleolithic diet first. Values ...Reported food intake

There were no period or carry-over effects in reported dietary intakes (data not shown). Reported daily food intake differed between diets mainly in that the Paleolithic diet was markedly lower in cereals and dairy products, and lower in potatoes, beans and bakery, and much higher in fruits, vegetables, meat and eggs (Table

(Table5).

5). Further, the Paleolithic diet was somewhat lower in total energy, energy density, carbohydrate, fiber, saturated fatty acids and calcium, and higher in monosaccharides, dietary cholesterol, some vitamins (vitamin B6, vitamin C, niacin) and minerals (potassium, selenium) (Table

(Table5).

5). During the Paleolithic diet, there was a lower relative intake (as a percentage of total macronutrient energy intake [E%]) of carbohydrate and a higher relative intake of protein and fat (Table

(Table5).

5). Both dietary GL and dietary GI were determined to be lower for the Paleolithic diet than for the Diabetic diet (Table

(Table5

5).

Table 5

Average food eaten per day during Paleolithic diet and Diabetes diet (mean ± SD)Exploratory analyses

In exploratory analyses of primary endpoints, within-subject differences (Δ) in HbA1c (ΔHbA1c) correlated with Δwaist circumference, which correlated with Δweight, which correlated with ΔCRP (Table

(Table6).

6). Furthermore, ΔHDL correlated with Δcholesterol and ΔDBP with ΔHOMA2 IR (Table

(Table6).

6). In exploratory analyses of estimated intake of nutrients, ΔHbA1c correlated with Δpotassium, ΔHDL with Δfatty acid C20:5 n-3, ΔTG with Δthiamin, ΔDBP with Δdietary cholesterol, Δweight with Δenergy density per meal, and Δwaist circumference with Δbakery, Δenergy density per meal, Δsauce and Δvitamin E (Table

(Table6

6).

Table 6

Exploratory analysesGo to:

Discussion

Key findings

The advice for patients with type 2 diabetes to follow a Paleolithic diet resulted in lower HbA1c, TG, DBP, weight and waist circumference, and higher HDL, as compared to a Diabetes diet according to current guidelines. In addition, fasting glucose and SBP tended to decrease more after the Paleolithic diet. Changes in glucose tolerance were not significantly different between diets. The two diets differed mainly in that the Paleolithic diet was lower in cereals and dairy products, and higher in fruits, vegetables, meat and eggs. Further, the Paleolithic diet was lower in total energy, energy density, carbohydrate, dietary GL, saturated fatty acids and calcium, and higher in unsaturated fatty acids, dietary cholesterol and several vitamins. Dietary GI was lower in the Paleolithic diet (GI = 50) than in the Diabetic diet (GI = 55).

Possible mechanisms and explanations

No advice was given to restrict food intake. Therefore, the lower reported energy intake during the Paleolithic diet despite no difference in weight of reported food intake agrees with the notion that such a diet is satiating and facilitates a reduced caloric intake [4,27]. Accordingly, energy density was lower in the Paleolithic diet and also correlated with alterations of both weight and waist circumference. The higher amount of fruit and vegetables during the Paleolithic period may have promoted weight loss due to its high content of water, which is thought to be satiating [28]. Interestingly, the Paleolithic diet appeared to be satiating despite a lower content of fiber in this study. The slightly higher relative protein intake, as percentage of total calorie intake, may also have added to a satiating effect [29,30]. Alternative explanations on satiation, such as dietary effects on leptin resistance, could also be considered [31].

A reduced energy intake would evidently be a major explanation for the beneficial effects of the Paleolithic diet on weight and waist circumference. Meta-analyses and large trials with various lifestyle interventions indicate that reduced caloric intake is more important for long-term weight loss than other known dietary factors, including macronutrient composition [32-40]. In studies shorter than 6 months, such as this one, differences in GI and/or GL may also have played a role for weight change. A Cochrane review found that overweight or obese people lost slightly more weight during 5–12 weeks of low GI diets [41], and short-term carbohydrate restriction possibly results in greater weight loss than low-fat diets [29]. However, dietary GI and dietary GL did not correlate with alterations of weight, waist circumference or metabolic variables in our study. It should also be noted that, in the present study, reported mean absolute carbohydrate intake in the Paleolithic diet (g per day) was only slightly below the 130 g per day recommended by the American Diabetes Association, and clearly above 50 g per day, which has been proposed as the level below which a diet should be termed a low carbohydrate diet [42].

Paleolithic diet improved the glycemic control in the subjects, as evident by the reduction of HbA1c levels by -0.4 percentage points lower as compared to the diabetes diet. Since both glucose and insulin levels declined during Paleolithic diet, a main mechanism behind the improved glycemic control is probably improved insulin sensitivity, which may have allowed the released insulin to work more efficiently. The difference in reduction in HbA1c of 0.4% units between the Paleolithic and Diabetes diet is close to the average 0.5% units in a recent Cochrane review of diets with a low glycemic index or glycemic load [8]. However, the differences in GI between diets in that meta-analysis were considerably larger than in our trial. Glucose tolerance, which also determines the glucose response and thereby HbA1c, did not improve more during the Paleolithic diet. This result agrees with findings from Frassetto et al [10], but differs from our previous parallel-group trial which compared a Paleolithic diet with a Mediterranean-like diet in subjects with diabetes or impaired glucose tolerance [4]. Glucose tolerance has not been shown to improve after reduced carbohydrate intake in earlier dietary studies [43-46].

The much higher fruit intake of the Paleolithic diet probably resulted in a slightly higher intake of fructose which may have aided in the reduction of HbA1c. Fructose in exchange for starch, sucrose or glucose decreases postprandial glycemia [47], while the effect on glucose tolerance and insulin sensitivity is more uncertain [48]. The effect of fruit on TG and other risk factors is expected to have been neutral in this study [48,49]. Total intake of monosaccharides was 46 g per day, including approximately equal amounts of glucose and fructose, which was well below the suggested safety limit of 50 g fructose per day [48]. Our study lends further support to the notion that fruit intake should not be restricted in patients with type 2 diabetes.

The lower DBP after the Paleolithic diet compared to the Diabetes diet did not correlate with sodium intake, which did not differ significantly and was rather low in both diets (2.5 g and 3.0 g per day respectively for the Paleolithic and Diabetes diet).

The reduction of TG after the Paleolithic diet was possibly due to greater loss of abdominal fat [50] or lower GL compared to the Diabetes diet [6], although no correlation of TG with waist loss or GL was seen in exploratory analyses. A small additional effect on TG may be attributable to a trend for higher content of long-chain omega-3 fatty acids in the Paleolithic diet, while the higher dietary cholesterol content of the Paleolithic diet is probably of minor significance [51].

Comparison with findings from other studies

All improvements in markers of the metabolic syndrome on the Paleolithic diet are in line with findings from epidemiological studies in non-Western populations [14-16]. Improvements in HbA1c [4], weight [4,12,52], BMI [52], waist circumference [4,52], DBP [10], and TG [10], compared to baseline, on a Paleolithic diet have been observed before in intervention studies, while improvements in HDL have not. Similar differences in weight and DBP on a Paleolithic diet, compared to a cereal based diet, have been observed before in an intervention study on domestic pigs [11]. A lower reported energy intake and energy density of food despite food intake ad libitum agrees with our earlier findings that a Paleolithic diet facilitates a reduction of caloric intake [4,11,27].

Also, lower intake of cereals, dairy products, carbohydrates, dietary GL and saturated fat, and higher intake of fruit and potassium have been observed before [4,10]. Lower intake of potatoes, bakery, fiber, phosphorous and calcium, and higher intake in vegetables, meat, eggs, monosaccharides, dietary cholesterol, vitamin B6, vitamin C, niacin and selenium have not been observed before in intervention studies with a Paleolithic diet. Dietary GI for a Paleolithic diet has not been determined before.

Limitations of the present study

A limitation of this study, as with most other dietary trials, is the lack of blinding after randomization. To minimize this problem, all study participants were informed of the intention to compare two healthy diets in the treatment of type 2 diabetes and that it was unknown if any of them would be superior to the other. Also, written information with dietary advice and food recipes were similarly formulated for both diets. Furthermore, for increased conformity, the dietary advice and data collection procedure were discussed by all those administering the interventions at several meetings prior to start of study.

Another limitation of this study is its small size which did not reach the number of participants needed as calculated in the pre-study power calculation. The decision to end the study was taken when recruitment for the study had not yielded new participants for more than six months. The population of patients with type 2 diabetes is much larger and therapy continues for substantially longer than in this study. Moreover, many patients with type 2 diabetes have illnesses and treatments that excluded them from the current study. Consequently, the results of this study do not address the occurrence of rare adverse events, nor can they be extrapolated to all patients seen in general clinical practice.

The carry-over effects on HbA1c were not due to carry-over or period effects in reported food intake. Instead, they could be true carry-over effects of the first diet. This is particularly likely for HbA1c, since HbA1c represents a weighted average of the blood glucose concentration over the previous two to three months ([53]. If results from the second period were discarded (owing to carryover [54]), the reduction of HbA1c from the Paleolithic diet compared to the Diabetes diet was still significant (p = 0.01) and even larger (-1.3% units) than when results from the second period were included. However, this approach could lead to biased answers to our hypothesis and results from both periods are therefore used in this study [54].

The lack of carry-over or period effects in reported food intake indicates fairly good adherence to intervention diets. Reported food intake in this study seemed reasonable both in distribution and quantity, as subjectively assessed by a nutrition engineer skilled in analyzing reported food intake (YG). Furthermore, the reported lower energy intake of 1.3 MJ per day on a Paleolithic diet equals about 3.2 kg fat during three months, which almost exactly accounts for the observed 3.3 kg difference in weight loss between diets. This indicates both good reporting by the participants and good adherence to reported food intake during the study.

Clinical and research implications

The favourable results in this study are in line with previous findings and increase the generalizability of the Paleolithic diet by testing it in both men and women in a primary care setting. A limitation of the study is the small size of the study population. This prevents the conclusions from resulting in nutritional recommendations for patients with type 2 diabetes. A long-term study in a larger population is therefore required. In parallel, further research into possible mechanisms for the beneficial effects of a Paleolithic diet should be done.

Total protein intake in g per day did not differ between the diets, but, as a result of the difference in total energy intake, the energy percentage (E%) from dietary protein on the Paleolithic diet (24 E%) slightly exceeded US and European recommendations for people with diabetes (<20 class="s1" e="" span="">17

,55]. The debatable disadvantage for long-term kidney function [56,57] should be weighed against the benefits of attenuated postprandial glycemia when protein replaces starch or glucose [58].

Calcium intake did not meet recommendations for any of the diets, and it was particularly low in the Paleolithic diet. Recent calcium balance studies indicate that human calcium requirements are lower than previously thought [59], and meta-analyses of randomized controlled trials suggest that the effect of calcium supplementation for bone strength is limited [60,61]. It has been suggested that absorption and excretion of calcium are more important than calcium intake for whole-body calcium balance [62]. In this context, the lower content of calcium-binding phytate and the lower dietary acid load from a Paleolithic diet may hypothetically compensate for the low amount of calcium [63]. Supporting this view are the findings of Frassetto et al, where calcium intake remained unchanged and urine calcium decreased after a Paleolithic diet compared to baseline [10].

As has been discussed, there may be a challenge to implement and adopt the Paleolithic diet on a worldwide scale in subjects with type 2 diabetes. However, this aspect is beyond the objective of this paper and requires more research.

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Conclusion

Based on the results of this 3-month randomized cross-over study in subjects with type 2 diabetes, a Paleolithic diet improves glycemic control in association with improvement of several cardiovascular risk factors compared to a conventional diabetes diet. The study supports the initiation of a large scale study on the effect of Paleolithic diet in subjects with type 2 diabetes.

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Competing interests

The authors declare that they have no competing interests.

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Authors' contributions

TJ participated in the design and execution of the study, participated in statistical analysis, and conceived of and wrote the article. YG analyzed reported food intake and participated in the design of the article as well as revising it for important intellectual content. BA participated in the design of the study, carried out the analysis of glucose and insulin in OGTTs, and revised the article for important intellectual content. UCB, GP, AH and MS participated in the design and execution of the study, and revised the article for important intellectual content. SL participated in the design of the study, participated in statistical analysis, and participated in the design of the article as well as revising it for important intellectual content. All authors read and approved the final manuscript.

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Acknowledgements

The authors are grateful to professor Birgitta Hovélius and Dr Kristina Haara for participation in designing the study, and to Lilian Bengtsson and Lena Kvist for technical assistance. The study was funded by Crafoordska stiftelsen, Region Skåne and Lund University.

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Articles from Cardiovascular Diabetology are provided here courtesy of BioMed Central

Asparagus Extract Tops Anti-Diabetes Drug Glibenclamide

Asparagus Extract Tops Anti-Diabetes Drug Glibenclamide. Plus: Dozens of Add. Health Benefits - From Aphrodisiac to Anti-Hangover & from Neuroprotection to Anti-Aging

Within the last couple of weeks, I have been moving news-items like this one into the "On Short Notice"  category, or simply totally discarded the dozen or so "herb XYZ" or "extract ABC ameliorates hypoglycemia in rodent model of type II diabetes" papers that are published on a weekly basis. The mere number of studies on whatever exotic, herb, spice or isolated polyphenol from the most remote areas (usually in Asia) the names of which I often even have heard about before, is simply too large to cover them all... and let's be honest: In the end, it's also downright boring to read about stuff that decreases blood glucose in a rodent model to a miniscule extend, when you already know that chances that you ever get your hands on a significant amount of that are zero, right? 

Coho salmon, shrimp and asparagus with melted butter - better than any diabetes drug ;-)

There are however, two good reasons, why Rahman Md. Hafizur, Nurul Kabir and Sidra Chishti most recent paper, which has been published on November 24 in the latest issue of the British Journal of Nutrition, has still made it not just into the short, but actually the 'official' SuppVersity news are twofold: Firstly, the effects of the Asparagus officinalis extract they administered at two different dosages to their rodents were just mediocre, but - as you are about to see - right on par with the diabetes drug glibenclamide, a sulfonylurea based medication that is often sold in combination with metformin (the respective drugs are called Glucovance and Glibomet). And secondly, briefly summarizing the main results of the study provided a nice incentive to dig somewhat deeper into the already established beneficial health effects of asparagus - and I can tell you, those are about as numerous as the aformentioned boring "herb XYZ"-studies ;-)

From the scientists' petri dishes to the rodent cage and... onto your dishes?

Asparagus officinalis L. is probably what the average Westerner would call "common asparagus". It's native to most European, African and Asian countries and its medicinal usage has been reported in the British and Indian Pharmacopoeias and in traditional systems of medicine such as Ayurveda, Unani and Siddha. Most of you will probably be aware of its mild diuretic effects and the distinct smell of your urine which will betray that you are someone who loves its delicate flavor in salads, vegetable dishes, soups and (if you are like me) poundwise with melted Kerrygold butter, some potatoes a decent amount of ham or some grilled meat during the asparagus season... but I am digressing here, let's get back to the facts.

To get to the bottom of previously reported beneficial effects of asparagus in various inflammatory (metabolic) diseases, the initially conducted an in-vitro study, to test the radical scavenging ability of their Asparagus extract and found that ...

"[...] A. officinalis at a concentration of 0·5 mg/ml exhibited 86·8 % radical-scavenging activity, as shown by a significant decrease in the absorbance of DPPH radicals. These results suggest that A. officinalis has potent antioxidant activity, as the positive control propyl gallate exhibited 91·4 % radical-scavenging activity. (Hafizur. 2012)

Afterwards they injected a group of male and female Wistar rats with streptozotocin to induce diabetes. Subsequently, the rodents received either 250 or 500mg/kg body weight of an Asparagus officinalis (AO) extract or 5mg/kg body weight of glibenclamide (GIB) once daily via an oral syringe - the dosage was adapted once weekly according to changes in body weight. 

Figure 1: Fasting blood glucose and insulin levels, total antioxidant status (TAS was measured using the ABTS) and beta cell area / islet expressed relative to control at the end of the 29 day study period (based on Hafizur. 2012)

A cursory glance at the data in figure 1 reveals: The initially betrayed anti-hypoglycemic effects (hypo[...] = ability to lower [blood sugar]) the high dose of Asparagus officinalis extract (AO500, figure 1) had on the fasting glucose levels of the animals were as potent as those of the diabetes drug glibenclamide.  Moreover, the treatment with AO500 had a slightly, but statistically significanty higher impact on the total antioxidant capacity and the same benificial effect on the morphology and function of the pancreas. Nevertheless, neither the A. officinalis extract, nor the glibenclamide treatment were able to restore the compromised insulin producton to more than ~70% of the value the non-streptozotocin-intoxicated animals.

There is much more to asparagus than it's antidiabetic effects 

As impressive as these results may be, if we simply rely on the findings Hafizur, Kabir and Chishtiit present in this recent paper, we will actually miss not just half, but rather 95% of the potential health benefits the different genus and parts of asparagus have to offer.

Figure 2: A. racemosis administered at a dose of 200mg/kg per day makes male rats about as horny (and able to perform) as bi-weekly injections of testosterone (Thakur. 2009) - not that you would need that, but it's nice to know anyways.

Despite the fact that asparagus is a highly nutritious source of vitamin B6, calcium, magnesium and zinc, and a very good source of dietary fiber, protein (in at least in view of the fact that it's an almost zero calorie veggie ;-), vitamin A, vitamin C, vitamin E, vitamin K, thiamin, riboflavin, rutin, niacin, folic acid, iron, phosphorus, potassium, copper, manganese, selenium, highly bioavailable chromium, and even small quantities omega-3 fatty acids (Morales. 2012), so that the regular incorporation of asparagus alone into your diet will supposedly be beneficial for you, some of the more intricate health effects may in fact require the extraction of and supplementation with specific phytonutrients from Asparagus officinalis, A. racemosus, A. cochinensis and its various cousins.

In order to give you an idea of what you can expect, I have compiled a comprehensive, yet by no means extensive list of benefits which have been ascribed to root, seed, and even leaf extracts of asparagus over the past decades 

• anti-cancer effects: Asparagus contains saponins that have in-vitro anti-(liver-)cancer effects (Ji. 2012); 
• neuroprotective effects: Chinese asparagus contains pregnanes that sooth neuro-inflammation (Jian. 2012; compounds could be present in regular A. officinalis as well) and can protect your liver and brain from aging (Xiong. 2011); 
• antiaging effects: A. contains enzymes that help with protein digestion (Ha. 2012); 
• hypolipidemic effects: n-butanol extracts from A. officinalis exert anti-hyperlipidemic effects (Zhu. 2011); 
• antimicrobial effects: A. has antibacterial activity against Escherichia coli, Shigella dysenteriae, Shigella sonnei, Shigella flexneri, Vibrio cholerae, Salmonella typhi, Salmonella typhimurium, Pseudomonas putida, Bacillus subtilis and Staphylococcus aureus (Mandal. 2000); 
• allows for geno-typing at home ;-) A. allows you to do a personal gene analysis to find out whether you have a single nucleotide polymorphism at rs4481887, which would make it impossible for you to smell the distinct odor the urine acquires after eating asparagus (Pelchat. 2011); 
• anti-hangover effects: A. helps your liver to metabolize alcohol and can even prevent a hangover (Kim. 2009); 
• buttery taste: A. contains phytochemicals which generate the sensation of having butter in the mouth (Dawid. 2012); 
• anti-stress effects: Ethanolic extracts from Asparagus racemosus have anti-stress activity and help your adrenals take a time out (Joshi. 2012)
• carbblocking effects: Asparagus racemosus inhibits the digestion of carbohydrates and enhances insulin action (Hannan. 2011); in this context it is interesting to remark that the in-vitro essay of the the study at hand suggested that A. officinalis, or rather the specific extract the scientists used in their study "has a very little effect on delaying glucose absorption" (Hafizur. 2012)
• immune promoting effects: A. racemosus ramps up natural killer cell activity (Thakur. 2012); AR also enhances memory and prevents amnesia (Ojha. 2012), 
• profound aphrodisiac effects: A dried root extract likewise from A. racemosus more than doubled the 'desire' of male rodents within 29 days (Thakur. 2009; cf. figure 2)
• MAO and acetylcholine breakdown inhibition: A. racemosus competitively inhibits acetylcholine and monoamine metabolizing enzymes (Meena. 2011)

As this highly incomplete list goes to show you, the health benefits are numerous. Unfortunately, this does also apply to the different phytochemicals which trigger all these effects. The probability that the next best extract you may find on the shelves or virtual outlets of a supplement store is actually going to to yield the health benefits you may be looking for are therefore pretty slim.

Although parts of it are edible as well, A. racemosus, is actually better known for its multitude of beneficial health effects that range from Antibacterial activity (some) antisecretory and antiulcer activity over mood enhancing and anti-depressive properties, and immunomodulatory effects to such profane things as libido enhancement or getting rid of superfluous water before a show or photo shoot.

Bottom line: In view of the practical problems associated with spotting appropriate extracts, I guess it would be best you take the fact that a 2003 paper in scientific journal Nutrition (Pellegrini. 2003) ranked asparagus 7th among 34 fruits and vegetables with respect to its free radical scavenging abilities, as an incentive to simply incorporate asparagus into your diets more frequently.

If, on the other hand, you are dealing with any specific health condition, it would certainly make sense to look for an extract that contains the proper genus of asparagus, is made from the right parts of the plant and - if possible - is even standardized for a specific compound: If you were interested in upping your estrogen levels, you would for example have to pick a whole plant extract of A. dumosus that would at best contain a standardized amount of 20-hydroxecysterone (Kaur. 1998). If it's rather the anti-ulcer effects you are after, your 'asparagus product of choice' should be made of the roots of A. racemosus ideally standardized for its Shatavairin content (Bhatnagar. 2005)... 

And now, you tell me eating healthy was complicated and taking supplements was easy ;-)

References

• Bhatnagar M, Sisodia SS, Bhatnagar R. Antiulcer and antioxidant activity of Asparagus racemosus Willd and Withania somnifera Dunal in rats. Ann N Y Acad Sci. 2005 Nov;1056:261-78.
• Dawid C, Hofmann T. Identification of Sensory-Active Phytochemicals in Asparagus (Asparagus officinalis L.). J Agric Food Chem. 2012 Nov 8.
• Ha M, Bekhit Ael-D, Carne A, Hopkins DL. Characterisation of kiwifruit and asparagus enzyme extracts, and their activities toward meat proteins. Food Chem. 2013 Jan 15;136(2):989-98. 
•  Hafizur RM, Kabir N, Chishti S. Asparagus officinalis extract controls blood glucose by improving insulin secretion and β-cell function in streptozotocin-induced type 2 diabetic rats. Br J Nutr. 2012 Nov;108(9):1586-95.
• Hannan JM, Ali L, Khaleque J, Akhter M, Flatt PR, Abdel-Wahab YH. Antihyperglycaemic activity of Asparagus racemosus roots is partly mediated by inhibition of carbohydrate digestion and absorption, and enhancement of cellular insulin action. Br J Nutr. 2011 Sep 8:1-8.
• Ji Y, Ji C, Yue L, Xu H. Saponins isolated from Asparagus induce apoptosis in human hepatoma cell line HepG2 through a mitochondrial-mediated pathway. Curr Oncol. 2012 Jul;19(Suppl 2):eS1-9.
• Jian R, Zeng KW, Li J, Li N, Jiang Y, Tu P. Anti-neuroinflammatory constituents from Asparagus cochinchinensis. Fitoterapia. 2012 Oct 24.
• Joshi T, Sah SP, Singh A. Antistress activity of ethanolic extract of Asparagus racemosus Willd roots in mice. Indian J Exp Biol. 2012 Jun;50(6):419-24. 
• Kaur H. Estrogenic activity of some herbal galactogogue constituents. Ind J Anim Nutr. 1998;5:232–4.
• Kim BY, Cui ZG, Lee SR, Kim SJ, Kang HK, Lee YK, Park DB. Effects of Asparagus officinalis extracts on liver cell toxicity and ethanol metabolism. J Food Sci. 2009 Sep;74(7):H204-8. 
• Meena J, Ojha R, Muruganandam AV, Krishnamurthy S. Asparagus racemosus competitively inhibits in vitro the acetylcholine and monoamine metabolizing enzymes. Neurosci Lett. 2011 Sep 26;503(1):6-9.
• Morales P, Ferreira IC, Carvalho AM, Sánchez-Mata MC, Cámara M, Tardío J. Fatty acids profiles of some Spanish wild vegetables. Food Sci Technol Int. 2012 Jun;18(3):281-90.
• Ojha R, Sahu AN, Muruganandam AV, Singh GK, Krishnamurthy S. Asparagus recemosus enhances memory and protects against amnesia in rodent models. Brain Cogn. 2010 Oct;74(1):1-9.
• Pelchat ML, Bykowski C, Duke FF, Reed DR. Excretion and perception of a characteristic odor in urine after asparagus ingestion: a psychophysical and genetic study. Chem Senses. 2011 Jan;36(1):9-17.
• Pellegrini N, Serafini M, Colombi B, Del Rio D, Salvatore S, Bianchi M, Brighenti F. Total antioxidant capacity of plant foods, beverages and oils consumed in Italy assessed by three different in vitro assays. J Nutr. 2003 Sep;133(9):2812-9. 
• Thakur M, Chauhan NS, Bhargava S, Dixit VK. A comparative study on aphrodisiac activity of some ayurvedic herbs in male albino rats. Arch Sex Behav. 2009 Dec;38(6):1009-15. Epub 2009 Jan 13.
• Thakur M, Connellan P, Deseo MA, Morris C, Praznik W, Loeppert R, Dixit VK. Characterization and in vitro immunomodulatory screening of fructo-oligosaccharides of Asparagus racemosus Willd. Int J Biol Macromol. 2012 Jan 1;50(1):77-81.
• Zhu X, Zhang W, Pang X, Wang J, Zhao J, Qu W. Hypolipidemic effect of n-butanol Extract from Asparagus officinalis L. in mice fed a high-fat diet. Phytother Res. 2011 Aug;25(8):1119-24.

The Grain That Damages The Human Brain

The Grain That Damages The Human Brain

Posted on: Friday, November 1st 2013 at 8:15 pm

Written By: Sayer Ji, Founder

With increasing recognition among medical professionals and the lay public alike that the health of gut and brain are intimately connected (i.e. the 'gut-brain' axis), the concept that gluten-containing grains can damage the human brain is beginning to be taken more seriously.  

Books like Dr. William Davis' New York Times best-selling Wheat Belly made great progress in opening up popular consciousness to the subject of gluten's addictive properties, my own e-book The Dark Side of Wheat explored the role that wheat and grains in general played as an addictive agent, and Dr. David Perlmutter's new book Grain Brain places significant emphasis on this connection as well. 

After all, if wheat is a common cause of intestinal damage ("enteropathy") both in those with celiac disease and non-celiac gluten sensitivity, it is no wonder that gluten-associated damage to the gut – sometimes called the "enteric brain," or "second brain," – could have adverse effects to the central nervous system as well.  

Indeed, our research project at GreenMedInfo.com has identified in biomedical literature directly from the National Library of Medicine over 200 adverse health effects linked to gluten-containing grains, with neurotoxicity top on the list of 21 distinct modes of toxicity associated with this grain's effects.[i]  These neurotoxic properties extend from neuropathy and ataxia, to distinct psychiatric conditions such as acute states of mania, and schizophrenia.

A recent study published in the Journal of Neurology, Neurosurgery and Psychiatry titled, "Hyperexcitable brain and refractory coeliac disease: a new syndrome," has identified a "new syndrome" within the broader array of so-called "gluten related disorders (GRD)" which the authors are calling "Hyperexcitable brain and refractory celiac disease."

According to the study, "Whilst coeliac disease (gluten sensitive enteropathy) remains one of the best characterised GRD, neurological dysfunction is one of the commonest extraintestinal manifestations with a range of presentations such as cerebellar ataxia, neuropathy, sensory ganglionopathy and encephalopathy (headaches and white matter abnormalities)."

They point out that neurological manifestations of gluten-induced toxicity can occur with or without evidence of intestinal damage (enteropathy). While wheat-induced intestinal damage is far more common than most suppose (read: Research Proves Wheat Can Cause Harm to Everyone's Intestines), the problem with gluten stretches far beyond the intestinal wall to so-called "out-of-intestine" adverse health effects. And given the fact that many of the peptide sequences within the vast array of proteins that we colloquially refer to as 'gluten' -- as if it were a singular entity versus the 23,000 plus proteins it is actually comprised of -- are pharmacologically psychoactive, it is no wonder that adverse neurological/cognitive consequences follow its ingestion. 

The new study describes a case study involving 7 patients (5 male, 2 female) who were identified from a cohort of 540 patients with neurological manifestations of "Gluten related disorders (GRD)." These patients showed signs of "myoclonic tremor," which is an involuntary muscle twitching, which initially occurred in their face, tongue, one arm or one leg, "but then spread to affect other parts of the body."  So severe was the tremor that 5 of the patients suffered from epileptic seizures, progressing from "Jacksonian seizures," a type of epilepsy that are initiated with abnormal electrical activity within the primary motor cortex, and may involve a wide range of behaviors from drooling, smacking of the lips, apparently purposeful movements such as turning of the head, etc. Furthermore, all the patients were described as having "limb ataxia and more prominent gait ataxia" – ataxia being a lack of voluntary coordination of muscle movements.

Electrophysiology 'brain tests' showed evidence of cortical myoclonus, which is defined as 'as involuntary brief muscle jerks originating from an abnormal discharge of the cerebral cortex.' Further clinical, imaging and/or pathological evaluation revealed some evidence of cerebellar involvement, but this was a secondary feature, distinguishing this new condition from gluten ataxia, where cerebellar ataxia is the most disabling feature.

All patients were made to adhere to a strict gluten-free diet, but even after eliminating gluten-related antibodies, there was still evidence of intestinal damage in keeping with so-called 'refractory' or treatment resistant celiac disease.  The researchers believe that this syndrome, while rare, is the commonest neurological manifestation of refractory celiac disease. They concluded:

"The clinical manifestations [of the newly named disorder] extend from focal reflex jerks to epilepsia partialis continua, covering the whole clinical spectrum of cortical myoclonus. This entity is possibly under-diagnosed and difficult to treat."

This study, of course, only addresses the small exposed tip of the massive Gluten-Related Disorder 'Iceberg'. But it does add renewed focus to the topic of wheat and gluten's brain-damaging and/or mind-altering properties.  Here are some additional studies linking wheat to brain issues:

• A high prevalence of gluten sensitivity is found in sporadic and hereditary cerebellar ataxia. A high prevalence of gluten sensitivity is found in sporadic and hereditary cerebellar ataxia. - Ann Neurol. 2001 Apr;49(4):540-3. PMID:
• Antigliadin antibodies are found at a higher prevalence in Cuban patients with spinocerebellar ataxia type 2. J Neurol Neurosurg Psychiatry. 2008 Mar ;79(3):315-7. Epub 2007 Oct 19.
• Antigliadin antibodies are found at a higher prevalence in Cuban patients with spinocerebellar ataxia type 2. J Neurol Neurosurg Psychiatry. 1999 Jan ;66(1):32-5.
• Epilepsy with cerebral calcifications of unexplained origin may likely be caused by undiagnosed celiac disease. Lancet. 1992 Aug 22;340(8817):439-43.
• Gluten sensitivity is a clinically confirmed problem in multiple sclerosis. Ann N Y Acad Sci. 2009 Sep;1173:343-9. Ann N Y Acad Sci. 2009 Sep;1173:343-9.
• Gluten sensitivity is associated with sporadic cerebellar ataxia in Taiwan.  Acta Neurol Taiwan. 2010 Dec;19(4):263-9.
• Headache and CNS white matter abnormalities may be associated with gluten sensitivity. Neurology. 2001 Feb 13 ;56(3):385-8.
• Highly significant increases compared with controls were found in patients with multiple sclerosis for IgA and IgG antibodies against gliadin and gluten and IgA antibodies against casein.  Acta Neurol Scand. 2004 Oct;110(4):239-41.
• Individuals with schizophrenia have a novel immune response to gluten. Schizophr Res. 2010 May;118(1-3):248-55. Epub 2009 Sep 11.
• Markers of gluten sensitivity and celiac disease are increased in recent-onset psychosis and multi-episode schizophrenia. Biol Psychiatry. 2010 Jul 1;68(1):100-4. Epub 2010 May 14.
• Neurological symptoms occur in 6-10% of those with celiac disease, with cerebella ataxia being the most frequent symptom. Mov Disord. 2009 Dec 15;24(16):2358-62.
• Persons with schizophrenia have higher than expected titers of antibodies related to celiac disease and gluten sensitivity.  Schizophr Bull. 2011 Jan;37(1):94-100. Epub 2009 Jun 3.
• Schizophr Bull. 2011 Jan;37(1):94-100. Epub 2009 Jun 3. Neurology. 2010 Sep 14;75(11):1003-8.
• There is a high prevlance of gluten sensitivity in Japanese patients with adult-onset cerebellar ataxia. Intern Med. 2006;45(3):135-40. Epub 2006 Mar 1.

So, what's the best way to find out if this research is accurate and relevant for you? My opinion is that the proof is in the gluten-free pudding. Try it out. Eliminate gluten-containing foods for a while, and see how you feel. Observe your memory, your cognition, etc. If it works, it works. If it doesn't, no harm done.

To learn more, watch Dr. Tom O' Bryan's short video on research indicating wheat ingestion can cut off blood flow to the brain.

[i] GreenMedInfo.com, Research > Substances > Index: A-Z > Wheat

Coconut oil miraculously helps Parkinson’s patient regain quality of life

Coconut oil miraculously helps Parkinson’s patient regain quality of life

Submitted by Alice Vaughn on October 23, 2013 – 4:18 pm

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Imagine for a moment that you are a 74-year-old man diagnosed with Parkinson’s disease, and you are quickly losing your ability to think, move and function, despite adhering to an intense regimen of all the latest pharmaceutical offerings for this miserable disease. Then imagine that nearly all of your symptoms subside almost miraculously after beginning a dietary routine that involves taking large doses of all-natural coconut oil every day.

Would you not tell the world about your amazing healing experience and encourage others in similar situations to do the same thing for their own health? This is what one older man did recently when he shared his powerful story , a question and answer support forum for people suffering from all sorts of illnesses and health conditions.

When drugs failed him, man adopted coconut oil regimen that changed his life

In a forum posting entitled “Coconut oil has improved my life,” the man, who identifies himself by the handle “fwes,” explains how his quality of life deteriorated quite rapidly after agreeing to undergo conventional treatment for Parkinson’s at the renowned Mayo Clinic. He explains how he had been taking drugs like Mirapex Er (pramipexole dihydrochloride), Azilect (rasagiline) and Sinemet (Carbidopa/Levodopa) to no avail.

His symptoms reportedly worsened on these drugs, leaving him in a state of catatonic pain and immobility. He describes his symptoms as including severe slowness, distorted facial expressions, chronic stiffness and joint pain, unsteadiness, severe swelling on his left leg and extreme lower back pain. These and many other symptoms are characteristic of late-stage Parkinson’s, and eventually lead to a total inability to take care of one’s self.

After three-and-a-half excruciating years of taking these multiple drugs for his condition and seeing no improvements, the man decided to take matters into his own hands. Research he discovered over at CoconutKetones.com, the blog of Dr. Mary Newport, M.D., led him to start taking coconut oil every day and building himself up to a tolerance of eight tablespoons daily. And the results were astounding.

Drastic improvements observed after just a few days on coconut oil

According to his personal account, the man experienced “significant improvements” after just a couple of days on the coconut oil. Family and friends were both shocked and delighted that he was suddenly able to move around the house quickly, for instance, and rise from any chair unassisted. He was also able to start performing what he describes as “football agility drills,” or shifting right and left and moving forward and backward in response to commands.

As long as he takes his coconut oil every day — four tablespoons at breakfast, two at lunch and two at dinner is his routine — then he experiences minimal symptoms and is able to go about his daily life in a mostly normal fashion. Besides improved agility and higher movement capacity, the man says his facial expressions have improved as a result of the coconut oil, and he no longer has any swelling on his left leg.

“I still have Parkinson['s] symptoms, but my quality of life has vastly improved,” he writes. “We are about at the end of 3 months, and the benefits are maintaining. Something real has happened to me.”

Source: http://www.naturalnews.com/042624_coconut_oil_Parkinsons_patient_quality_of_life.html#ixzz2iYNkJqUw

The Roles of Iodine in the Body • Maintaining the Thyroid

The Roles of Iodine in the Body • Maintaining the Thyroid

August 14, 2013 by Michael Ravensthorpe Filed Under: Nutrient Profiles Tagged With: Nutrients

Iodine is a chemical element that is mainly found on Earth as a water-soluble ion, meaning that it tends to concentrate in oceans and saltwater pools. This element – which our bodies cannot make, meaning we need to derive it from food – is perhaps best-known for its role in maintaining thyroid function, which is an extremely important task. In fact, it’s not an exaggeration to say that iodine is needed for the healthy functioning of practically every cell in our bodies. Let’s take a closer look at those functions.

What Iodine Does for Us

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Maintains thyroid function – Iodine helps our bodies to produce thyroid hormones, which ensure that our thyroid remains healthy. The thyroid is a large endocrine gland located near the base of the neck that controls how quickly our bodies use energy, create proteins, and regulate hormone sensitivity. An underactive thyroid slows the metabolism, making weight loss difficult. Therefore, a healthy thyroid is the first requisite for a successful weight loss diet.

Promotes physical and mental growth – Iodine is especially important for children because the thyroid hormones it produces are closely related to growth hormones, which are needed for both physical and mental growth. Consequently, an iodine deficiency can result in both physical retardation and the retardation of intelligence and basic skills such as speech, movement, and hearing. These issues also extend towards unborn children; studies at the Linus Pauling Institute, for instance, have shown that an iodine deficiency during pregnancy can cause mental retardation and stunted growth in the baby. Iodine deficiencies have even been shown to increase the risk of stillbirth, miscarriage, and birth defects.

Regulates body temperature – Thyroid hormones help our bodies to dilate our blood vessels, thus allowing warm blood to flow to our extremities. This means that our body temperatures are greatly influenced by our iodine intake. When our iodine levels are comfortable, our cells make more energy, resulting in increased body temperature. Conversely, when our iodine levels are low, our body temperature decreases, and we experience cold hands and feet.

Controls cholesterol and heart rate – The thyroid hormone triiodothyronine (T3) helps us to trigger the breakdown of cholesterol, resulting in reduced cholesterol levels. The T3 hormone also controls our heartbeat rate; too much iodine results in a fast heartbeat, which tires the heart, while too little iodine results in a poor circulation of oxygen, nutrients, and warmth. Ideally, you want your heart to beat at around 72 beats per minute, which is what you’re likely to have if your diet contains good amounts of iodine.

Maintains a healthy emotional state – Since thyroid hormones affect our sensitivity to adrenaline and other endocrine hormones, insufficient thyroid hormone levels (induced by insufficient iodine levels) effectively limits our ability to respond to events in a normal manner. This can lead to lethargy and apathy (the feeling of being ‘dead inside’ can be caused by an iodine deficiency). In some cases, it can trigger full-blown depression.

Recommended Daily Intake

The RDI of iodine for adolescents and adults of both sexes is 150 micrograms per day. Young children (between 1-8 years) should receive 90 micrograms per day, while older children (between 9-13 years) should receive 120 micrograms per day. The RDI of iodine for pregnant women, on the other hand, is 220 micrograms per day, increasing to 270 micrograms per day for breastfeeding women.

Just Say No: When It Makes Sense Not to Take Your Medicine

Just Say No: When It Makes Sense Not to Take Your Medicine

By Joseph Mercola

Mercola.com

October 31, 2013

By Dr. Mercola

You’ve probably heard the advice that eating healthier, exercising and relieving your stress – all facets of a healthy lifestyle – can help you to prevent and even treat diseases.

But perhaps you haven’t really taken it to heart. The problem is that this knowledge doesn’t always translate into actions, and rather than starting an exercise program or drinking a freshly prepared green vegetable juice, many visit their physicians and receive a prescription for medication.

Even many physicians neglect to tell their patients about the simple and, oftentimes, free changes they can make to dramatically improve their health, simply because they have been brainwashed by the conventional system and are convinced that drugs are part of the, if not the sole, answer for virtually any health condition.

Sometimes It Is Better to Skip the Medication

There are clearly some cases where medications are useful and even lifesaving. I am not opposed to medication – provided it is used correctly and only when necessary. And that latter point is key. Medications are often promoted as necessary when they actually aren’t.

Take type 2 diabetes. A new systematic review and meta-analysis combed through data of nine randomized, controlled trials of patients who were at risk of developing diabetes.

The study revealed that ‘comprehensive lifestyle interventions,’ which included factors like exercise and dietary changes, effectively decreased the incidence of type 2 diabetes in high-risk patients.1

Or consider cancer. Another study found that women who walked, cut their breast cancer risk by 14 percent, and those who exercised vigorously cut it by 25 percent, compared to those who didn’t exercise.2 Similarly, men with prostate cancer had more longer-lived cells if they ate right, managed their stress and lead healthy lifestyles.3

And in one particularly revealing study, researchers found that simply being married was associated with significantly greater survival among people with cancer, compared to those who were separated, divorced, widowed or never married.

The implication is that social support appears to have a large impact on your ability to survive a disease, and this study even found that the survival benefits of marriage for cancer patients were greater than those from chemotherapy!4

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Still, the dangerous misconception persists in the US, among both patients and physicians, that when you’re sick you virtually always need a drug to feel better.

Examples of additional health problems that typically don’t require drug intervention include short-term conditions like colds and flu, headaches and minor aches and pains to chronic conditions like:

• Heart disease
• High blood pressure
• High cholesterol
• Insomnia

• Certain mental health problems

Be Prepared: The ‘Health Care’ System Is Set Up to Prescribe Drugs

The business of being a doctor in the US has been largely reduced to being the front man for a multi-billion dollar drug business whose primary mission seems to be enriching their bottom line by keeping you sick and dependent on drugs to relieve — but not cure — your health complaints.

The system is carefully orchestrated to sell the quick fix, the drug, and that is precisely why so many Americans equate prescription medications with wellness. In reality, in many cases, the “cure” merely adds new problems to a patient’s list of complaints…

During your last appointment with a physician of any sort, specialist or primary care, what happened?

• Did you have a discussion about diet, exercise, nutrition, eating plans, sleep or stress management? 
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• Were you cautioned not to consume too much refined sugar or flour, trans fats or processed meats?
• Were you given advice on natural supplements or lifestyle changes that can help you achieve optimal health?

Or did the entire appointment simply address the symptoms you came in with or a screening for an illness you might have? And did it end with the doctor giving you a prescription? Unless your physician specializes in nutrition or holistic medicine, the prescription was probably the main focus of your appointment. That’s because treating symptoms and diseases — and prescribing drugs for them — is what modern doctors are trained to do. As reported in TIME:5

“The U.S. health care system is designed to react to disease and treat it once symptoms set in — the reimbursement structure is founded on doctors diagnosing problems and treating them, for example, most often with medications. ‘The focus of our system is embedded in disease treatment. People make a lot of money off the way it was built, so we give lip service to prevention. But exercise is free.’”

Do You Really Know the Power of a Healthy Lifestyle?

I regularly scour news feeds to find out about the latest research that may be relevant to improving health, so I’m continually amazed and impressed by the power of lifestyle interventions. But perhaps you haven’t heard some of the recent revelations that show just how powerful a player your lifestyle is in your overall health.

Consider:

• A growing body of research suggests there may be a powerful connection between the foods you eat and your risk of Alzheimer’s disease and dementia, via similar pathways that cause type 2 diabetes.
• Chronic stress results in alterations in your brain-gut connection, which can cause or worsen numerous gastrointestinal disorders, including inflammatory bowel disease, irritable bowel syndrome, food allergies, GERD and more. 
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• Exercise is one of the safest, most effective ways to prevent and treat chronic diseases such as heart disease. After reviewing 305 randomized controlled trials, researchers found no statistically detectable differences between physical activity and medications, such as statins and beta-blockers, for pre-diabetes and heart disease.6

• Practicing mindfulness meditation for just four days affects pain responses in your brain. Brain activity decreases in areas devoted to monitoring a painful body part and also in areas responsible for relaying sensory information.

Not to Mention, Medications Can Be Deadly

No one wants to treat any disease only to find that their treatment has caused a new problem that may be even worse than their initial disease… but prescription drugs now kill more people than illegal drugs. Death by prescription drugs is a 21st century epidemic, now killing even more Americans than motor vehicle accidents.

Drug fatalities more than doubled for teens and young adults between 2000 and 2008, and more than tripled among people age 50 to 69. It’s estimated there are 450,000 preventable adverse events related to medications in the US every year, accounting for a substantial proportion of emergency room visits. And when you add in deaths from hospital-acquired infections, unnecessary medical procedures, and adverse surgical outcomes, conventional medicine should top the list of theleading causes of death in the US. The average annual prescription rate for children, adults and seniors in the US is now:7

• More than 4 prescriptions per child (age 0-18)
• Nearly 12 prescriptions per adult
• 28 prescriptions per senior, aged 65 and over

Does this sound excessive to you? If so, it’s important to remember that you are the only one who can be fully responsible for your health. You can choose to believe that this responsibility rests on someone else’s shoulders, but at the end of the day, you are the one

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who has to live with the consequences, for better or worse. This is why some of the most important common-sense questions you need to ask before you take any drug include:

• Do I really need it?
• What are the alternatives? (lifestyle-based or otherwise)
• Is it prescribed appropriately, or is it being prescribed for an off-label use?
• What are the side effects? (Both common and uncommon side effects)

• Is it addictive and is it known to interact with any other drugs, supplements, or foods that I’m taking?

Ready? Set… Go! Take Control of Your Health

Viewing drugs as a last resort rather than a first-line defense will go a long way toward keeping you healthy, as will embracing positive lifestyle choices. You CAN take control of your health, and this trend appears to be catching on. TIME reported on one excellent program being used by New York City physicians to encourage patients to eat more produce:8

“At Lincoln Medical Center and Harlem Hospital in New York City, doctors are starting to focus more on prevention by making diet changes a priority for patients — before they find themselves diagnosed with a disease like diabetes or heart trouble. The hospitals have launched the Fruit and Vegetable Prescription, a four-month pilot program, which allows patients with prescriptions — written by their doctors — to get coupons for fresh produce at farmers’ markets and the city’s green carts.”

It certainly helps to have a physician who thinks beyond drugs… but if yours doesn’t, it’s up to you to find one who does. And it’s also up to you to embrace the healthy lifestyle that can make you feel better. An excellent starting point is my free nutrition plan, which virtually anyone can follow starting right now. What are you waiting for? TIME summed it up well:9

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“It’s not that prescription medicines… don’t have a place in modern medicine. They do… But if it’s possible to avoid disease altogether, and if patients can do it without expensive medications that can cause complications, why wouldn’t they? Wouldn’t you?”

Sources and References

• Annals of Internal Medicine October 15, 2013
• TIME October 16, 2013

• 1 Annals of Internal Medicine October 15, 2013
• 2 Cancer Epidemiol Biomarkers Prev. 2013 Oct;22(10):1906-12
• 3 Lancet Oncol. 2013 Oct;14(11):1112-20.
• 4 J Clin Oncol. 2013 Sep 23.
• 5 TIME October 16, 2013
• 6 British Medical Journal 2013;347:f5577
• 7 Kaiser Family Foundation, Retail Prescription Drugs Filled at Pharmacies, 2011
• 8 TIME October 16, 2013
• 9 TIME October 16, 2013

Sleep Is Critical for Brain Detoxification, Groundbreaking Research Finds

Sleep Is Critical for Brain Detoxification, Groundbreaking Research Finds

October 31, 2013 | 133,944 views

Visit the Mercola Video Library

By Dr. Mercola

Scientists have long tried to tease out the purpose of sleep, and countless studies have concluded that sleep is deeply interconnected with your health in a myriad of ways. As just one example, previous research has found that sleep deprivation has the same effect on your immune system as physical stress or illness.1

Quite simply, even if you do everything else right, if you don’t sleep enough, your health and well-being will still suffer. You may even die prematurely, should poor sleep plague you long-term.

Now, researchers at the University of Rochester Medical Center (URMC) Center for Translational Neuromedicine believe they may have discovered yet another clue as to why sleep is mandatory for good health—especially brain health.

Their report, published in the journal Science,2 reveals that your brain has a unique method of removing toxic waste through what’s been dubbed the glymphatic system.3, 4, 5, 6, 7

The clincher is that this system ramps up its activity during sleep, thereby allowing your brain to clear out toxins, including harmful proteins linked to brain disorders such as Alzheimer’s for example.

What’s more, they discovered that your brain cells actually shrink by about 60 percent during sleep, which allows for more efficient waste removal. According to lead author Maiken Nedergaard, M.D., D.M.Sc., featured in the video above:

“This study shows that the brain has different functional states when asleep and when awake. In fact, the restorative nature of sleep appears to be the result of the active clearance of the by-products of neural activity that accumulate during wakefulness.”

What Is the Glymphatic System?

In your body, the lymphatic system is the system responsible for eliminating cellular waste products. However, the lymphatic system does not include your brain. The reason for this is that your brain is a closed system, protected by the blood-brain barrier, which controls what can go through and what cannot.

In a previous animal study,8 Dr. Nedergaard showed that the brain actually has its own unique waste disposal system, similar to that of the lymphatic system. This system, called the glymphatic system, “piggybacks” on the blood vessels in your brain. The “g” in glymphatic is a nod to “glial cells”—the brain cells that manage this system.

By pumping cerebral spinal fluid through your brain’s tissues, the glymphatic system flushes the waste, from your brain, back into your body’s circulatory system. From there, the waste eventually reaches your liver, where it’s ultimately eliminated.

During sleep, the glymphatic system becomes 10 times more active than during wakefulness. Simultaneously, your brain cells are reduced in size by about 60 percent.

This creates more space in-between the cells, giving the cerebrospinal fluid more space to flush out the debris. Amyloid-beta, for example—proteins that form the notorious plaque found in the brains of Alzheimer’s patients—is removed in significantly greater quantities during sleep. As stated by Time Magazine:9

“The findings raise interesting questions about how sleep may affect the progression of Alzheimer’s or other neurogenerative disorders, but they also provide a strong warning for anybody who skips sleep. The short version: don’t.”

According to Dr. Nedergaard:10

“The brain only has limited energy at its disposal and it appears that it must choose between two different functional states — awake and aware or asleep and cleaning up. You can think of it like having a house party. You can either entertain the guests or clean up the house, but you can’t really do both at the same time.

...These findings have significant implications for treating ‘dirty brain’ disease like Alzheimer’s. Understanding precisely how and when the brain activates the glymphatic system and clears waste is a critical first step in efforts to potentially modulate this system and make it work more efficiently.”

How Sleep Influences Your Physical Health

Sleep is usually one of the first things people sacrifice when the going gets tough, and this could be a critical mistake. First of all, significant memory impairment can occur after a single night of poor sleep—meaning sleeping only 4 to 6 hours. It also has a detrimental impact on your ability to think clearly the next day, and decreases your problem solving ability.

But foggy-headedness and forgetfulness are the least of your worries should you ignore your poor sleeping habits. Aside from impacting your immune function as briefly mentioned earlier, poor sleep is now known to have multi-varied detrimental effects on your health, courtesy of your circadian system, which "drives" the rhythms of biological activity at the cellular level. Disruptions to this biological clock tend to cascade outward throughout your entire body.  For example, interrupted or impaired sleep can:

Increase your risk of heart disease.11	Harm your brain by halting new cell production. Sleep deprivation can increase levels of corticosterone (a stress hormone), resulting in fewer new brain cells being created in your hippocampus.
Impair your ability to lose excess pounds or maintain your ideal weight. This is likely the effect of altered metabolism, because when you’re sleep deprived, leptin (the hormone that signals satiety) falls, while ghrelin (which signals hunger) rises.	Contribute to a pre-diabetic state, making you feel hungry even if you've already eaten, which can wreak havoc on your weight.
Accelerate tumor growth, primarily due to disrupted melatonin production. Melatonin inhibits the proliferation of a wide range of cancer cell types, as well as triggering cancer cell apoptosis (self destruction). The hormone also interferes with the new blood supply tumors require for their rapid growth (angiogenesis)	Contribute to premature aging by interfering with your growth hormone production, normally released by your pituitary gland during deep sleep (and during certain types of exercise, such as high intensity interval training).
Raise your blood pressure.	Increase your risk of dying from any cause.

Furthermore, lack of sleep can further exacerbate chronic diseases such as:

Parkinson's	Alzheimer's	Multiple Sclerosis (MS)
Gastrointestinal tract disorders	Kidney disease	Behavioral problems in children

Why You Shouldn’t Reach For a Sleeping Pill When You Can’t Sleep...

Chronic lack of sleep has a cumulative effect when it comes to disrupting your health, so you can’t skimp on sleep on weekdays, thinking you’ll “catch up” over the weekend. You need consistency. Generally speaking, adults need between six and eight hours of sleep every night. There are plenty of exceptions though. Some people might need as little as five hours a night, while others cannot function optimally unless they get nine or 10 hours.

My strong recommendation and advice is quite simply to listen to your body. If you feel tired when you wake up, you probably need more sleep. Frequent yawning throughout the day is another dead giveaway that you need more shut-eye. Personally, I find that when I am reading during the day, if my eyes close and I tend to doze off, I know I did not get enough sleep the night before. However, above all, should insomnia strike, don’t make the mistake of reaching for a sleeping pill.

Not only do sleeping pills not address any of the underlying causes of insomnia, researchers have repeatedly shown that sleeping pills don’t work, but your brain is being tricked into thinking they do... One analysis found that, on average, sleeping pills help people fall asleep approximately 10 minutes sooner, and increase total sleep time by a mere 15-20 minutes. They also discovered that while most sleeping pills caused poor, fragmented sleep, they induced amnesia, so upon waking, the participants could not recall how poorly they’d actually slept!

In terms of health consequences, this could end up being worse than not sleeping and being aware of that fact. At least then you’d be encouraged to find and address the root cause of your sleeplessness. Besides not working as advertised, sleeping pills have also been linked to significant adverse health effects, including a nearly four-fold increase in the risk of death, and a 35 percent increased risk of cancer.

How to Optimize Your Sleep

Below are half a dozen of my top guidelines for promoting good sleep. For a comprehensive sleep guide, please see my article "33 Secrets to a Good Night's Sleep."

1. Avoid watching TV or using your computer at night—or at least about an hour or so before going to bed—as these technologies can have a significantly detrimental impact on your sleep. TV and computer screens emit blue light; nearly identical to the light you're exposed to outdoors during the day. This tricks your brain into thinking it's still daytime, thereby shutting down melatonin secretion.
2. Under normal circumstances, your brain starts secreting melatonin between 9 or 10 pm, which makes you sleepy. When this natural secretion cycle is disrupted, due to excessive light exposure after sunset, insomnia can ensue.
3. Sleep in complete darkness, or as close to it as possible. Even the slightest bit of light in the room can disrupt your internal clock and your pineal gland's production of melatonin and serotonin. So close your bedroom door, and get rid of night-lights. Refrain from turning on any light at all during the night, even when getting up to go to the bathroom. Cover up your clock radio.
4. Make sure to cover your windows—I recommend using blackout shades or drapes.
5. Keep the temperature in your bedroom no higher than 70 degrees F. Many people keep their homes and particularly their upstairs bedrooms too warm. Studies show that the optimal room temperature for sleep is between 60 to 68 degrees. Keeping your room cooler or hotter can lead to restless sleep. This is because when you sleep, your body's internal temperature drops to its lowest level, generally about four hours after you fall asleep. Scientists believe a cooler bedroom may therefore be most conducive to sleep, since it mimics your body's natural temperature drop.
6. Take a hot bath 90 to 120 minutes before bedtime. This increases your core body temperature, and when you get out of the bath it abruptly drops, signaling your body that you are ready for sleep.
7. Check your bedroom for electro-magnetic fields (EMFs). These can disrupt your pineal gland and the production of melatonin and serotonin, and may have other negative effects as well. To do this, you need a gauss meter. You can find various models online, starting around $50 to $200. Some experts even recommend pulling your circuit breaker before bed to shut down all power in your house.
8. Move alarm clocks and other electrical devices away from your bed. If these devices must be used, keep them as far away from your bed as possible, preferably at least three feet. This serves at least two functions. First, it can be stressful to see the time when you can't fall asleep, or wake up in the middle of the night. Secondly, the glow from a clock radio can be enough to suppress melatonin production and interfere with your sleep. Cell phones, cordless phones and their charging stations should ideally be kept three rooms away from your bedroom to prevent harmful EMFs.

Sleeping Well Is Part of a Healthy Lifestyle Plan

There's convincing evidence showing that if you do not sleep enough, you're really jeopardizing your health. Everybody loses sleep here and there, and your body can adjust for temporary shortcomings. But if you develop a chronic pattern of sleeping less than five or six hours a night, then you're increasing your risk of a number of health conditions, including weakening your immune system and increasing your risk of degenerative brain disorders. If you’re feeling anxious or restless, try using the Emotional Freedom Techniques (EFT), which can help you address any emotional issues that might keep you tossing and turning at night.

For even more helpful guidance on how to improve your sleep, please review my 33 Secrets to a Good Night's Sleep. If you're even slightly sleep deprived, I encourage you to implement some of these tips tonight, as high-quality sleep is one of the most important factors in your health and quality of life.