Thursday, 22 December 2011

40 Things You Should Know – The Science (part 2)

Points 1-7

A randomized trial of a hypocaloric high-protein diet, with and without exercise, on weight loss, fitness, and markers of the Metabolic Syndrome in overweight and obese women.

http://www.ncbi.nlm.nih.gov/pubmed/17622289

Abstract

The purpose of this study was to examine the effects of 3:1 and 1:1 carbohydrate to protein ratios, hypocaloric diets with and without exercise, and risk factors associated with the Metabolic Syndrome in overweight and obese Canadian women. Groups were designated as control diet (CON), control diet with exercise (CONEx), high-protein (HP), or high-protein with exercise (HPEx). Free-living women from the Guelph community were studied in a university health and fitness facility. The participants were 44 of 60 overweight and obese women who had been randomized to the 4 weight-loss programs. Habitual diets of the subjects were energy restricted and were to contain either a 1:1 or 3:1 ratio of carbohydrate to protein energy. Subjects either exercised 3 times/week or maintained their normal level of activity for 12 weeks. The main outcome measures were weight loss, blood lipids, blood pressure, insulin, body composition, nitrogen balance, fitness, and resting energy expenditure. All groups lost weight over the 12 week period: -2.1 kg for the CON group, -4.0 kg in the CONEx group, -4.6 kg in the HP group, and -7.0 kg in the HPEx. All participants exhibited improved body composition, decreased blood pressure, and decreased waist and hip circumference. Actual diets consumed by the subjects contained ratios of carbohydrate to protein of 3.0:1, 2.7:1, 1.5:1, and 0.96:1 for the CON, CONEx, HP, and HPEx groups, respectively. Cardiovascular fitness improved in both exercise groups. There were no changes in resting energy expenditure. No adverse events were reported. Significant changes in blood lipids included decreased total cholesterol in the HP and CONEx groups, decreased low-density lipoprotein cholesterol in the HP group only, and decreased blood triglycerides in the HPEx group only. High-density lipoprotein cholesterol, fasting blood glucose, and fasting insulin levels were unaltered by diet or exercise. A high-protein diet was superior to a low-fat, high-carbohydrate diet either alone or when combined with an aerobic/resistance-training program in promoting weight loss and nitrogen balance, while similarly improving body composition and risk factors for the Metabolic Syndrome in overweight and obese Canadian women.

 

A carbohydrate-restricted diet during resistance training promotes more favorable changes in body composition and markers of health in obese women with and without insulin resistance.

http://www.ncbi.nlm.nih.gov/pubmed/21673483

Abstract

Objective:


To determine whether sedentary obese women with elevated levels of homeostatic model assessment (HOMA) insulin resistance (ie, > 3.5) experience greater benefits from an exercise + higher-carbohydrate (HC) or carbohydrate-restricted weight loss program than women with lower HOMA levels.


Methods:


221 women (age, 46.5 ± 12 years; body weight, 90.3 ± 16 kg; body mass index, 33.8 ± 5 kg/m(2)) participated in a 10-week supervised exercise and weight loss program. The fitness program involved 30 minutes of circuit-style resistance training 3 days per week. Subjects were prescribed low-fat (30%) isoenergetic diets that consisted of 1200 kcals per day for 1 week (phase 1) and 1600 kcals per day for 9 weeks (phase 2) with HC or higher protein (HP). Fasting blood samples, body composition, anthropometry, resting energy expenditure, and fitness measurements were obtained at 0 and 10 weeks. Subjects were retrospectively stratified into lower (LH) or higher (HH) than 3.5 HOMA groups. Data were analyzed by multivariate analysis of variance with repeated measures and are presented as mean ± standard deviation changes from baseline.


Results:


Baseline HOMA levels in the LH group were significantly lower than those in the HH group (LH, 0.6 ± 0.7; HH, 6.3 ± 3.4; P = 0.001). Diet and training significantly decreased body weight (-3.5 ± 3 kg), fat mass (-2.7 ± 3 kg), blood glucose (-3%), total cholesterol (-4.5%), low-density lipoproteins (-5%), triglycerides (-5.9%), systolic blood pressure (-2.6%), and waist circumference (-3.7%), while increasing peak aerobic capacity (7.3%). Subjects in the HP group experienced greater weight loss (-4.4 ± 3.6 kg vs -2.6 ± 2.9 kg), fat loss (-3.4 ± 2.7 kg vs -1.7 ± 2.0 kg), reductions in serum glucose (3% vs 2%), and decreases in serum leptin levels (-30.8% vs -10.8%) than those in the HC group. Participants in the HH (-14.1%) and HP-HH (-21.6%) groups observed the greatest reduction in serum blood glucose.


Conclusions


 A carbohydrate-restricted diet promoted more favorable changes in weight loss, fat loss, and markers of health in obese women who initiated an exercise program compared with a diet higher in carbohydrate. Additionally, obese women who initiated training and dieting with higher HOMA levels experienced greater reductions in blood glucose following an HP diet.


A high-protein diet with resistance exercise training improves weight loss and body composition in overweight and obese patients with type 2 diabetes.

http://care.diabetesjournals.org/content/33/5/969.long

Abstract

OBJECTIVE


To evaluate the effects of two low-fat hypocaloric diets differing in the carbohydrate-to-protein ratio, with and without resistance exercise training (RT), on weight loss, body composition, and cardiovascular disease (CVD) risk outcomes in overweight/obese patients with type 2 diabetes. RESEARCH DESIGN AND METHODS A total of 83 men and women with type 2 diabetes (aged 56.1 +/- 7.5 years, BMI 35.4 +/- 4.6 kg/m(2)) were randomly assigned to an isocaloric, energy-restricted diet (female subjects 6 MJ/day, male subjects 7 MJ/day) of either standard carbohydrate (CON; carbohydrate:protein:fat 53:19:26) or high protein (HP; 43:33:22), with or without supervised RT (3 days/week) for 16 weeks. Body weight and composition, waist circumference (WC), and cardiometabolic risk markers were assessed.


RESULTS


Fifty-nine participants completed the study. There was a significant group effect (P <or= 0.04) for body weight, fat mass, and WC with the greatest reductions occurring in HP+RT (weight [CON: -8.6 +/- 4.6 kg, HP: -9.0 +/- 4.8 kg, CON+RT: -10.5 +/- 5.1 kg, HP+RT: -13.8 +/- 6.0 kg], fat mass [CON: -6.4 +/- 3.4 kg, HP: -6.7 +/- 4.0 kg, CON+RT: -7.9 +/- 3.7 kg, HP+RT: -11.1 +/- 3.7 kg], and WC [CON: -8.2 +/- 4.6 cm, HP: -8.9 +/- 3.9 cm, CON+RT: -11.3 +/- 4.6 cm, HP+RT: -13.7 +/- 4.6 cm]). There was an overall reduction (P < 0.001) in fat-free mass (-2.0 +/- 2.3 kg), blood pressure (-15/8 +/- 10/6 mmHg), glucose (-2.1 +/- 2.2 mmol/l), insulin (-4.7 +/- 5.4 mU/l), A1C (-1.25 +/- 0.94%), triglycerides (-0.47 +/- 0.81 mmol/l), total cholesterol (-0.67 +/- 0.69 mmol/l), and LDL cholesterol (-0.37 +/- 0.53 mmol/l), with no difference between groups (P >or= 0.17).


Conclusions


An energy-restricted HP diet combined with RT achieved greater weight loss and more favorable changes in body composition. All treatments had similar improvements in glycemic control and CVD risk markers.


Increased protein intake reduces lean body mass loss during weight loss in athletes.

http://www.ncbi.nlm.nih.gov/pubmed/19927027

Abstract

PURPOSE:

To examine the influence of dietary protein on lean body mass loss and performance during short-term hypoenergetic weight loss in athletes.

METHODS:

In a parallel design, 20 young healthy resistance-trained athletes were examined for energy expenditure for 1 wk and fed a mixed diet (15% protein, 100% energy) in the second week followed by a hypoenergetic diet (60% of the habitual energy intake), containing either 15% (approximately 1.0 g x kg(-1)) protein (control group, n = 10; CP) or 35% (approximately 2.3 g x kg(-1)) protein (high-protein group, n = 10; HP) for 2 wk. Subjects continued their habitual training throughout the study. Total, lean body, and fat mass, performance (squat jump, maximal isometric leg extension, one-repetition maximum (1RM) bench press, muscle endurance bench press, and 30-s Wingate test) and fasting blood samples (glucose, nonesterified fatty acids (NEFA), glycerol, urea, cortisol, free testosterone, free Insulin-like growth factor-1 (IGF-1), and growth hormone), and psychologic measures were examined at the end of each of the 4 wk.

RESULTS:

Total (-3.0 +/- 0.4 and -1.5 +/- 0.3 kg for the CP and HP, respectively, P = 0.036) and lean body mass loss (-1.6 +/- 0.3 and -0.3 +/- 0.3 kg, P = 0.006) were significantly larger in the CP compared with those in the HP. Fat loss, performance, and most blood parameters were not influenced by the diet. Urea was higher in HP, and NEFA and urea showed a group x time interaction. Fatigue ratings and "worse than normal" scores on the Daily Analysis of Life Demands for Athletes were higher in HP.

CONCLUSIONS:

These results indicate that approximately 2.3 g x kg(-1) or approximately 35% protein was significantly superior to approximately 1.0 g x kg(-1) or approximately 15% energy protein for maintenance of lean body mass in young healthy athletes during short-term hypoenergetic weight loss.




Effect of two different weight-loss rates on body composition and strength and power-related performance in elite athletes.

 

http://www.ncbi.nlm.nih.gov/pubmed/21558571

 

Abstract

When weight loss (WL) is necessary, athletes are advised to accomplish it gradually, at a rate of 0.5-1 kg/wk. However, it is possible that losing 0.5 kg/wk is better than 1 kg/wk in terms of preserving lean body mass (LBM) and performance. The aim of this study was to compare changes in body composition, strength, and power during a weekly body-weight (BW) loss of 0.7% slow reduction (SR) vs. 1.4% fast reduction (FR). We hypothesized that the faster WL regimen would result in more detrimental effects on both LBM and strength-related performance. Twenty-four athletes were randomized to SR (n = 13, 24 ± 3 yr, 71.9 ± 12.7 kg) or FR (n = 11, 22 ± 5 yr, 74.8 ± 11.7 kg). They followed energy-restricted diets promoting the predetermined weekly WL. All athletes included 4 resistance-training sessions/wk in their usual training regimen. The mean times spent in intervention for SR and FR were 8.5 ± 2.2 and 5.3 ± 0.9 wk, respectively (p < .001). BW, body composition (DEXA), 1-repetition-maximum (1RM) tests, 40-m sprint, and countermovement jump were measured before and after intervention. Energy intake was reduced by 19% ± 2% and 30% ± 4% in SR and FR, respectively (p = .003). BW and fat mass decreased in both SR and FR by 5.6% ± 0.8% and 5.5% ± 0.7% (0.7% ± 0.8% vs. 1.0% ± 0.4%/wk) and 31% ± 3% and 21 ± 4%, respectively. LBM increased in SR by 2.1% ± 0.4% (p < .001), whereas it was unchanged in FR (-0.2% ± 0.7%), with significant differences between groups (p < .01). In conclusion, data from this study suggest that athletes who want to gain LBM and increase 1RM strength during a WL period combined with strength training should aim for a weekly BW loss of 0.7%.

Strength and neuromuscular adaptation following one, four, and eight sets of high intensity resistance exercise in trained males

http://www.ncbi.nlm.nih.gov/pubmed/21451937


Abstract

The optimal volume of resistance exercise to prescribe for trained individuals is unclear. The purpose of this study was to randomly assign resistance trained individuals to 6-weeks of squat exercise, prescribed at 80% of a 1 repetition-maximum (1-RM), using either one, four, or eight sets of repetitions to failure performed twice per week. Participants then performed the same peaking program for 4-weeks. Squat 1-RM, quadriceps muscle activation, and contractile rate of force development (RFD) were measured before, during, and after the training program. 32 resistance-trained male participants completed the 10-week program. Squat 1-RM was significantly increased for all groups after 6 and 10-weeks of training (P < 0.05). The 8-set group was significantly stronger than the 1-set group after 3-weeks of training (7.9% difference,P < 0.05), and remained stronger after 6 and 10-weeks of training (P < 0.05). Peak muscle activation did not change during the study. Early (30, 50 ms) and peak RFD was significantly decreased for all groups after 6 and 10-weeks of training (P < 0.05). Peak isometric force output did not change for any group. The results of this study support resistance exercise prescription in excess of 4-sets (i.e. 8-sets) for faster and greater strength gains as compared to 1-set training. Common neuromuscular changes are attributed to high intensity squats (80% 1-RM) combined with a repetition to failure prescription. This prescription may not be useful for sports application owing to decreased early and peak RFD. Individual responsiveness to 1-set of training should be evaluated in the first 3-weeks of training.

Muscular adaptations in response to three different resistance-training regimens: specificity of repetition maximum training zones.

http://www.ncbi.nlm.nih.gov/pubmed/12436270

Abstract

Thirty-two untrained men [mean (SD) age 22.5 (5.8) years, height 178.3 (7.2) cm, body mass 77.8 (11.9) kg] participated in an 8-week progressive resistance-training program to investigate the "strength-endurance continuum". Subjects were divided into four groups: a low repetition group (Low Rep, n = 9) performing 3-5 repetitions maximum (RM) for four sets of each exercise with 3 min rest between sets and exercises, an intermediate repetition group (Int Rep, n = 11) performing 9-11 RM for three sets with 2 min rest, a high repetition group (High Rep, n = 7) performing 20-28 RM for two sets with 1 min rest, and a non-exercising control group (Con, n = 5). Three exercises (leg press, squat, and knee extension) were performed 2 days/week for the first 4 weeks and 3 days/week for the final 4 weeks. Maximal strength [one repetition maximum, 1RM), local muscular endurance (maximal number of repetitions performed with 60% of 1RM), and various cardiorespiratory parameters (e.g., maximum oxygen consumption, pulmonary ventilation, maximal aerobic power, time to exhaustion) were assessed at the beginning and end of the study. In addition, pre- and post-training muscle biopsy samples were analyzed for fiber-type composition, cross-sectional area, myosin heavy chain (MHC) content, and capillarization. Maximal strength improved significantly more for the Low Rep group compared to the other training groups, and the maximal number of repetitions at 60% 1RM improved the most for the High Rep group. In addition, maximal aerobic power and time to exhaustion significantly increased at the end of the study for only the High Rep group. All three major fiber types (types I, IIA, and IIB) hypertrophied for the Low Rep and Int Rep groups, whereas no significant increases were demonstrated for either the High Rep or Con groups. However, the percentage of type IIB fibers decreased, with a concomitant increase in IIAB fibers for all three resistance-trained groups. These fiber-type conversions were supported by a significant decrease in MHCIIb accompanied by a significant increase in MHCIIa. No significant changes in fiber-type composition were found in the control samples. Although all three training regimens resulted in similar fiber-type transformations (IIB to IIA), the low to intermediate repetition resistance-training programs induced a greater hypertrophic effect compared to the high repetition regimen. The High Rep group, however, appeared better adapted for submaximal, prolonged contractions, with significant increases after training in aerobic power and time to exhaustion. Thus, low and intermediate RM training appears to induce similar muscular adaptations, at least after short-term training in previously untrained subjects. Overall, however, these data demonstrate that both physical performance and the associated physiological adaptations are linked to the intensity and number of repetitions performed, and thus lend support to the "strength-endurance continuum".

40 Things You Should Know – The Science (part 1)

Ok so this ended being a little longer than anticipated. After putting together all the research and study abstracts, it turned out to be 48 pages of text and over 16,000 words! I will be breaking it up in a few sub parts so it will be easier to read and navigate.

This first part I have linked a number of articles and research reviews that directly relate d to some of  the ’40 Things You Should Know’ points.

I could have linked many more especially from Lyle McDonald’s site but chose only to do a couple of articles but the majority are his research review of a number of research papers (some of which I have used). Alan Aragon, Emma-Leigh Synnott, Martin Berkhan and Jamie Hale have helped in a great way with this and allowing me access to their work, articles and research reviews.

For more in-depth articles I suggest you check out their websites.


Emma-Leigh Synnott - http://www.emma-leigh.com/

Martin Berkhan - http://www.leangains.com/



Here we go , enjoy!

Point 40


Point 42



Point 1, 16, 21, 22, 26, 32, 34, 37




Point 35


Point 5, 6, 7, 10





Point 30



Point 33


Point 33, 34




Point 27
http://www.bodyrecomposition.com/research-review/glycaemic-index-effects-on-fuel-partitioning-in-humans.html


http://alanaragon.com/elements-challenging-the-validity-of-the-glycemic-index.html




Point 21, 22, 24, 25



Point 1, 21, 22

Point 21, 22, 25


Point 15



Point 46



Point 16, 17, 18, 23, 24

Point 31

Tuesday, 13 December 2011

40 Things You Should Know – The one liners.


Ok so this is a two part series that will (hopefully) explain the actual facts, basics and fundamentals behind achieving your desired body composition, exercise performance and general health goals.

It may very well be the complete opposite to what you have seen, heard or do.

So this first part is essentially the ‘one liners’ that are the facts, basics or fundamentals behind it all.  Yes I do realize some are more than one line but one liners sounds better (LOL).

Part 2 will be the science behind it and all the studies that prove it.

Body Composition

Minus lifestyle factors (smoking, sleep patterns, stress) and hereditary factors (illness or diseases).

1.       Calorie surplus = weight gain.  Calorie deficit = weight loss. Meal frequency does not alter the energy balance equation. 

2.       Calorie intake, macronutrient and micronutrient sufficiency determines health NOT food name or type and NOT meal frequency.

3.       Activity + calorie intake, macronutrient and micronutrient sufficiency determines vitality NOT food name or type and NOT meal frequency.

4.       Calorie intake, macronutrient and micronutrient sufficiency determines the activity level ability NOT food name or type and NOT meal frequency.

5.       Long term activity stimuli, calorie intake and macronutrient sufficiency determines body composition NOT food name or type and NOT meal frequency or day to day intake.

6.       Body composition progression requires continual increase in activity stimuli load, appropriate calorie intake and macronutrient sufficiency NOT food name or type and NOT meal frequency.

7.       Activity stimuli progression requires activity load increase, appropriate calorie intake, sufficient macronutrient and micronutrient intake NOT food name or type and NOT meal frequency.

Training

8.       Being sore after a workout does not determine whether the workout was good or not.

9.       Having a pump does not determine if a workout was good or not.

10.   Training progression is what determines if the workout was good or not.

11.   The only way you ‘shock’ the body into growth is to continually increase the activity stimuli load NOT by changing exercises around or doing different exercises.

12.   You can grow muscle.  Muscle tone is girly for muscle growth.  You can’t shape muscle.  Muscle shape is genetic.  You can shape muscle by making it grow.

13.   Abs are achieved by having a low body fat NOT by doing abdominal crunches.

14.   X-Fit is for fitness not muscle growth or gain.

15.   Cardio means cardiovascular exercise NOT fat burning exercise. It actually burns 3 times more carbohydrates regardless of intensity!

Nutrition & Random

16.   Calorie = a unit to measure energy.

17.   Macronutrient = Protein, Carbohydrate and Fat.

18.   Micronutrient = Vitamins and Minerals.

19.   Consuming your daily required calories, macronutrients and micronutrients is far more important than nutrient timing.

20.   The ‘anabolic window’ is a 24-48 hour window not a 30 minute or a 2 hour window.

21.   A calorie is a calorie.

22.  Calories in VS Calories out always applies.

23.   One gram of protein is 4 calories.  One gram of carbohydrate is 4 calories.  One gram of fat is 9 calories.

24.   One gram of protein, carbohydrate and fat is no different between food types and is still the same calorie value.  Our body sees nutrients NOT food names or types. Ratios of protein, carbohydrate and fats (and micronutrients) may vary between food type that is all.

25.   Foods should not be classed as clean or dirty.  If you wash your food, then it is clean.

26.   Carbohydrates at night do not make you fat.  Being in a calorie surplus does.

27.   GI is meaningless in a mixed diet.

28.   Unless you have multiple muscle glycogen depletion workouts in the same day for the same muscle group/s, replenishing muscle glycogen directly post workout is unnecessary.

29.  Insulin is spiked anytime you eat/consume nutrients. Spiking insulin around training with 'simple carbohydrates' is unnecessary.

30.   You can absorb more than 30 grams of protein in one meal.

31.   Protein does not kill your kidneys.

32.   Fat does not make you fat.  Being in a calorie surplus does.

33.   You do not have a fast or slow metabolism. Everyone has a different metabolic function which is determined by a number of different factors (see next point). It should not be classed as fast, slow, high or low. It should have no classification. You can not use that as an excuse,  you just consume too little or too many calories.

34.   Your TEE (Total energy expendature/calorie requirements) is determined by BMR - Base Metabolic Rate (age, gender, lean body mass, overall bodyweight etc etc), NEAT (non exercise associated thermogenesis), EAT (exercise associated thermogenesis) and TEF (thermic effect feeding). TEF is determined by macronutrient balance/intake NOT meal frequency.

35.   Hunger/appetite does not reflect a particular metabolism type.  Feeding frequency, macronutrient balance and hormonal function control hunger/appetite levels.

36.   We are continually in both catabolic and anabolic states.  We have no control over that.

37.   Increased meal frequency does not alter nor have an effect on energy balance.

38.   Supplements supplement your diet.  Diet does not supplement your supplements.

39.   Placebo is real.

40.   Supplements are not steroids.  Steroids are steroids. Supplements will NOT give you steroid like results regardless of the marketing. 

* Note:  If you have any more suggestions please let me know. If I think of something I may have missed. I will update it along the way.

The forgotten Ones

41.  A calorie deficit can be achieved  either dietary or activity induced or a combination of the two.

42.  Studies can prove or disprove anything. The funding source, credibility and methods used in a study prove everything about a study.

43.   Only studies done on humans need be considered. We are not rats, mice or dogs.

44.  Saturated fat is NOT bad nor is Cholesterol.

45. Rocky was a movie. You are not Rocky and you are not in a movie. Cook your damn eggs, do not drink them raw. You can not digest a raw egg, you are not that tough.

46.  Because a 'Pro' does something that is not evidence to base a theory or argument on. The physique does not determine the intelligence level.

47.  Creatine is NOT a steroid.

48. Your metabolism will NOT slow down if you have not eaten in 3 hours or 4 or 5 etc etc, try 60 hours without food!

49. Caffeine and creatine can be take together. They do NOT  'counter act' each other.

50. Caffeine does NOT dehydrate you nor have a negative effect on electrolyte balance .

 

Monday, 12 December 2011

Aspartame and Sucralose – You’re on trial for murder! Or is that really the case?


No it is not the case at all!  *waits for the shit-storm to start*…

I’m going to do this a little differently and I’m going to say my part now as an overview and then break down all the sweeteners with the scientific studies and the conclusions/findings.

With that said, some things are just jumped on more than others and the subject of sweeteners is one the bandwagon jumpers love.

I look at it like this.  Nearly everything that is promoted either by mainstream media/nutrition is typically based on the absolute EXTREME of the situation at hand and rarely actually applies to the majority of the population.  Also there is always a bias behind why something is promoted - government and industry based.  Funding of studies and advertising campaigns are rarely done out of the kindness of one’s heart.  I will probably make that cross-reference many more times in future articles!

Take the sweetener Aspartame for example which is derived from the amino acid Phenylalanine (and Aspartic Acid).  For individuals who suffer from Phenylketonuria it can and does cause massive problems.  It is very toxic to those individuals and can cause problems with brain development, leading to progressive mental retardation, brain damage, and seizures (1).

Phenylketonuria is a disease that is associated with a particular enzyme that metabolizes Phenylalanine into Tyrosine in the brain.  It is a genetic disorder, meaning you can’t acquire it later in life, you are born with it.  
Now with that in mind, for healthy individuals there is no need to worry or avoid consumption of Aspartame (or others for that matter).  The researchers know that and have explained that time and time again.  It has been approved for consumption etc, yet due to the fact is affects a certain population, mainstream media and misguided nutritional ‘experts’ (I use that term extremely loosely) pigeonhole it as bad, dangerous and unhealthy blah blah blah.

What really amuses me is that while Aspartame is ‘bad’ (for people with Phenylketonuria) and everyone must avoid it, bananas have MORE Phenylalanine than what is found in Aspartame!  Yet you do not hear ANYONE say bananas are ‘bad’ and should be avoided.  Also if you drink protein shakes or eat protein from whole food you are consuming more Phenylalanine than what is in a diet soft drink.

Just off topic for a moment, the same can be applied to people with nut allergies.  It can be deadly for those individuals yet you never hear nuts being promoted as bad.

I do realize there are other sweeteners on the market (i.e. Stevia) and to be completely honest, the actual available scientific data with human subjects is limited at best.  Most studies, and the subsequent intake recommendations, are based on tests on animal subjects.   (I’ll touch on that in a second).  So with that in mind, I’d suggest that safe ranges for consumption should be as per the suggested amount in the RDI tables (credible or not as they are).

Take it for what it is.  If you do not have a health issue that is directly linked to a certain nutrient or the like, there is no need to avoid it just because it affects a particular population that YOU are not a part of.
I must make mention that there are a number of studies on headaches and the consumption of sweeteners with most showing mixed results (2,3).  So as mentioned, if that is the trigger for YOU, limiting your consumption may be required.  If it is not you, continue as normal.

Also if you do find a study done on rats or mice that shows a negative effect, that is fine because we are not rats, we are not mice and we should only be concerned with human studies and the data from them.

Here is a breakdown of your typical sweeteners and the actual facts:

Aspartame   –

Aspartame: review of safety. http://www.ncbi.nlm.nih.gov/pubmed/12180494
The safety testing of Aspartame has gone well beyond that required to evaluate the safety of a food additive.  When all the research on Aspartame is examined as a whole, including evaluations in both the pre-marketing and post-marketing periods, it is clear that Aspartame is safe and there are no unresolved questions regarding its safety under conditions of intended use.

Aspartame: a safety evaluation based on current use levels, regulations, and toxicological and epidemiological studies.  http://www.ncbi.nlm.nih.gov/pubmed/17828671

Epidemiological studies on Aspartame include several case-control studies and one well-conducted prospective epidemiological study with a large cohort, in which the consumption of Aspartame was measured.  The studies provide no evidence to support an association between Aspartame and cancer in any tissue.  The weight of existing evidence is that Aspartame is safe at current levels of consumption as a non-nutritive sweetener.


Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects. http://www.ajcn.org/content/68/3/531.long


Plasma Phenylalanine concentrations increased significantly during Aspartame treatment. Neuropsychologic results; adverse experiences; amino acid, insulin, and glucose values; and electroencephalograms were compared by sex and by treatment. No significant differences were found for any dependent measure.
CONCLUSION: Large daily doses of Aspartame had no effect on neuropsychologic, neurophysiologic, or behavioral functioning in healthy young adults.


Effect of Aspartame and sucrose loading in glutamate-susceptible subjects.
Plasma Phenylalanine and Aspartate levels were similar to those noted in normal subjects administered identical doses of Aspartame.  The data indicates no effect of Aspartame loading in glutamate-susceptible subjects.

Sucralose  -

An overview of the safety of sucralose. http://www.ncbi.nlm.nih.gov/pubmed/19464334


The collective evidence supports the conclusion that the ingredient, sucralose, is safe for use in food and that the sucralose-mixture product, Granulated SPLENDA No Calorie Sweetener, is also safe for its intended use.


Repeated dose study of sucralose tolerance in human subjects.

http://www.ncbi.nlm.nih.gov/pubmed/10882825

Based on these studies and the extensive animal safety database, there is no indication that adverse effects on human health would occur from frequent or long-term exposure to sucralose at the maximum anticipated levels of intake.


Effects of oral ingestion of sucralose on gut hormone response and appetite in healthy normal-weight subjects. http://www.ncbi.nlm.nih.gov/pubmed/21245879

Oral ingestion of sucralose does not increase plasma GLP-1 or PYY concentrations and hence, does not reduce appetite in healthy subjects. Oral stimulation with sucralose had no effect on GLP-1, insulin or appetite.


Sucralose metabolism and pharmacokinetics in man. http://www.ncbi.nlm.nih.gov/pubmed/10882816

The radiolabelled material present in faeces was essentially unchanged sucralose.



For a great informal discussion and loads of information I’d suggest checking out this link - http://forum.bodybuilding.com/showthread.php?t=291569&page=1

References -