Pesticides could be responsible for Parkinson's, a neurodegenerative disease.
Toxins from such chemicals can increase the risk by up to six times.
The seven pesticides tested include: dithiocarbamates (e.g., maneb, ziram), two imidazoles (benomyl, triflumizole), two dicarboxymides (captan, folpet), and one organochlorine (dieldrin)

This study was done at the University of California at Los Angeles (UCLA).
The study clearly revealed that these seven toxic pesticides inhibit the aldehyde dehydrogenase (ALDH) enzyme, which then affects the dopamine cells linked to the development of Parkinson's.
It has been well established in the medical arena that when dopamine levels decrease this results in abnormal brain activity and eventually to the signs of Parkinson's.
Of even greater concern, the scientists of this study reported that the pesticides caused an inhibition of the ALDH enzyme at far lower levels than the allowable current safety standards.
Although one of the pesticides (benomyl) has been banned, the others can still be found in everyday use. They are found in the foods we eat that have been sprayed with these toxic chemicals and found in parks and golf courses. They are also found in common pesticide control agents used in offices and homes.
As a functional medicine practitioner, I recommend that any patient suffering with Parkinson's request that their physician order the Toxic Effects Core test or the GPL-TOX Profile from Great Plains Lab
To find a healthcare professional certified in functional medicine, go to www.FunctionalMedicineDoctors.com.These are clinicians who have been trained at Functional Medicine University (www.FunctionalMedicineUniversity.com)


Written by: Ronald Grisanti D.C., D.A.B.C.O., D.A.C.B.N., M.S.

Reference:
Arthur G. Fitzmaurice, PhD*, Shannon L. Rhodes, PhD*, Myles Cockburn, PhD,  Beate Ritz, MD, PhD and Jeff M. Bronstein, MD, PhD. Aldehyde dehydrogenase variation enhances effect of pesticides associated with Parkinson disease. Neurology February 4, 2014 vol. 82 no. 5 419-426
https://ehp.niehs.nih.gov/doi/10.1289/isee.2013.P-3-23-13
The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the research and experience of Dr. Grisanti and his functional medicine community. Dr. Grisanti encourages you to make your own health care decisions based upon your research and in partnership with a qualified health care professional. Visit www.FunctionalMedicineUniversity.com for more information on our training in functional medicine. 

Walnuts have been shown to improve memory, cognition and neuronal effects related to oxidative stress (OS) and inflammation (INF) in animals and human trials.
Walnut looks like the brain, has a left and right hemisphere, upper cerebrums and lower cerebellums. The folds and wrinkles of a walnut resembles to human organ: the brain. The shape of the nut even approximates the body part, looking like it has left and right hemispheres. And it's no surprise walnuts are nicknamed "brain food"—they have a very high content of omega-3 fatty acids, which help support brain function." The wrinkles and folds mimic the neo-cortex.
​Walnuts develop over three dozen neuron-transmitters for brain function. They may also help head off dementia. Recent study found that walnut extract broke down the protein-based plaques associated with Alzheimer's disease. They found walnuts reversed some signs of brain aging in rats. Walnuts also appear to enhance signaling within the brain and encourage new messaging links between brain cells
Fibrillar amyloid beta-protein (Abeta) is the principal component of amyloid plaques in the brains of patients with Alzheimer's disease. Scientific studies suggest that walnuts may reduce the risk or delay the onset of Alzheimer's disease by maintaining Abeta in the soluble form. Basically, walnuts had inhibited Abeta fibrillization. It is proposed that polyphenolic compounds (such as flavonoids) present in walnuts may be responsible for its anti-amyloidogenic activity.
To find a healthcare professional certified in functional medicine, go to www.FunctionalMedicineDoctors.com.These are clinicians who have been trained at Functional Medicine University (www.FunctionalMedicineUniversity.com)

Written by: Ronald Grisanti D.C., D.A.B.C.O., D.A.C.B.N., MS
References:
Poulose SM1, Miller MG, Shukitt-Hale B.,Role of walnuts in maintaining brain health with age. J Nutr. 2014 Apr;144
Poulose SM1, Bielinski DF, Shukitt-Hale B. Walnut diet reduces accumulation of polyubiquitinated proteins and inflammation in the brain of aged rats. J Nutr Biochem. 2013 May;24(5):912-9
Chauhan N1, Wang KC, Wegiel J, Malik MN. Walnut extract inhibits the fibrillization of amyloid beta-protein, and also defibrillizes its preformed fibrils. Curr Alzheimer Res. 2004 Aug;1(3):183-8.
The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the research and experience of Dr. Grisanti and his functional medicine community. Dr. Grisanti encourages you to make your own health care decisions based upon your research and in partnership with a qualified health care professional. Visit www.FunctionalMedicineUniversity.com for more information on our training in functional medicine. 

If you suffer from insomnia then you understand the seriousness of simply not getting a good night's sleep. Your whole world around you appears to crumble when you can't get a good 6-8 hours of quality deep REM sleep. Your work life, your family life all suffer.
Today's article will touch on a few "key" things to consider to solve insomnia.
To begin remember that the awakening after a few hours of sleep and not being able to get back to sleep is often rebound from what you ate or drank hours before. High sugar, alcohol, highly spiced foods and of course, caffeinated drinks are often the culprits.
If you are unknowingly deficient in chromium, vanadium, manganese and other nutrients you can experience hypoglycemic rebound in a few hours where you abruptly wake-up and are unable to drift back to sleep.
Let's now consider something called the “happy hormones” that lead to a restful sleep.
One of these hormones is serotonin, which anti-depressants like Prozac work on.
We make serotonin from the amino acid tryptophan.
Unfortunately as we age or faced with an overload of stress the level of serotonin suffers.
Dozens of studies show that low tryptophan levels lead to insomnia, awakening feeling unrested, inability to stay asleep after getting there, and just lying there all night watching the clock.
For over a quarter of a century literally dozens of studies have proven this amino produces a great sleep in many, and with no side effects or hangover. In fact, folks have better mental clarity during the day. Furthermore, it improves daytime depression, PMS, fibromyalgia, and anxiety as well as carbohydrate cravings, binge-eating and even alcohol recovery.
Now from a functional medicine position it is important to know that a simple B6 or zinc deficiency can contribute to insomnia. A common vitamin B6 deficiency can keep you awake all night, or low zinc causing impaired conversion of B6, which is needed to make tryptophan work.
If you have an elevated organic acid, kynurenate acid, for example, and a low tryptophan, the correction of B6 may be all you need.
Now don't forget plasticizers in our bodies lower zinc which is needed in the enzyme to convert B6 to its active form so it can then transform tryptophan to a serotonin.
I am disappointed with the number of people suffering with insomnia who could be helped if only their physician understood the significance of nutritional biochemistry.
It comes down to finding the cause of the cause.
Remember that as important as serotonin is for sleep and moods, most of serotonin is not made in the brain.
Ninety five percent of serotonin is made in the gut.
If the gut isn't healthy, then you are going nowhere. If you have gas, bloating, alternating diarrhea or constipation or other gut issues than your chances of solving your insomnia problem may be futile until you fix your gut.
The secret is to find a doctor who understands the probable underlying causes of insomnia and knows how to do the proper testing to discover what needs to be fixed.
It really can be as simple as that.

By: Ronald Grisanti D.C., D.A.B.C.O., D.A.C.B.N., M.S.
​
References
Schmidt HS, L-tryptophan in the treatment of impaired respiration in sleep, Bull Eur Physiopathol Respir, 19; 6:625-9, 1983
Demisch K, et al, Treatment of severe chronic insomnia with Ltryptophan: results of a double-blind cross-over study, Pharmocopsychiatry, 20; 6:242-4, 1987
Hartmann E, Effects of L-tryptophan on sleepiness and on sleep, J Psychiatr Res, 17; 2:1-7-13, 1982
Ashley DV, et al, Evidence for diminished brain 5-hydroxytrptamine biosynthesis in obese diabetic and non-diabetic humans, Am J Clin Nutr, 42; 6:1240-5, 1985
Riemann D, et al, The tryptophan depletion test: impact on sleep in primary insomnia - a pilot study, Psychiatry Res, 109; 2:129-35, 2002
Schneider-Helmert D, et al, Evaluation of L-tryptophan for treatment of insomnia: a review, Psychopharmacol (Berl), 89; 1:1-7, 1986
 
 
The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the research and experience of Dr. Grisanti and his community. Dr. Grisanti encourages you to make your own health care decisions based upon your research and in partnership with a qualified health care professional.

​
A recent patient was concerned that despite watching her diet and taking her diabetes medication her hemoglobin A1C (HbA1c) keeps going up.
Remember, HbA1c is a lab test that shows the average level of blood sugar (glucose) over the previous 3 months. It shows how well you are controlling your diabetes. 
An elevated HbA1c greater than 5.7% indicates that the diabetes is not well regulated and is in fact accelerating aging, increasing your chances of getting painful neuropathies, kidney failure needing dialysis, cataracts, amputations, and retinopathy blindness.
What could possibly be missed by her primary doctor?
One major cause of the unregulated glycosylated hemoglobin is an unrecognized B6 deficiency.


An excellent “functional” test to check for a pyridoxine (B-6) deficiency is the xanthurenate organic acid test. An elevated xanthurenate test is a sensitive marker for a B-6 deficiency.
 

​
This is an Organic Acid Test from Genova


But wait.. there is more to the story.
You can take B-6 and it may not work.
Why?
Because of a zinc deficiency.
When hidden zinc deficiency is present, the body cannot convert B6 to its active form, pyridoxal-5-phosphate or P5P. P5P, essential in normalizing the glycosylated hemoglobin and its deficiency, is an indicator that improperly metabolized sugars are accelerating aging, cataracts, kidney failure, heart disease, nerve damage and more.


But there is more to the story.
Elevated stored phthalates (plastics) in the body interfere with zinc metabolism


This is the power of functional medicine. Seeking to find the cause of the cause of the cause.
HbA1c ---> B-6 deficiency ---> Zinc deficiency ---> Stored Phthalates
I have never yet met a diabetologist who even orders the above much less knows how to interpret it.
To ignore fixing the chemistry in an overtly metabolic disease is outright wrong.
Unfortunately, what I have seen from reading thousands of medical records is the fact that most doctors merely resort to the one size fits all approach and medicate the disease. Rarely if ever have I read where a doctor investigated why the HA1C was elevated.
This results in a tragic waste of life as well as incurring an enormous and unnecessary expense and suffering.
You may be interested to know that because of the phthalate load, many folks (even without diabetes) unnecessarily get multiple diseases. These can range from Nonalcoholic steatohepatitis or NASH (a common, often “silent” liver disease), heart disease or cancers to Parkinson's disease, arthritis, or Alzheimer's.
Clearly they all lead to accelerated aging because of the shared causes.
For a doctor to check your glycosylated hemoglobin A1C every 3 months yet never know your zinc and B6 levels (among many others) is plain wrong in this sophisticated era.
Your life depends on the decisions you make. This information has a huge bearing on whether your diabetes blinds you in future years.
 
Written by: Ronald Grisanti D.C., D.A.B.C.O., D.A.C.B.N., M.S.

References:
Depeint F, et al, Mitochondrial function and toxicity: Role of B vitamins, one-carbon transfer pathways, Chemico-Biological Interactions 163:113-32, 2006
Jain SK, et al, Pyridoxine and pyridoxamine inhibits superoxide radicals and prevents lipid peroxidation, protein glycosylation and (Na+ + K+)-ATPase activity reduction in high glucose-treated human erythrocytes, Free Rad Biol Med 30:232-37, 2001
Onarato JM, et al, Pyridoxamine, an inhibitor of glycation reactions, also inhibits lipid peroxidation reactions, J Biol Chem, 275:21177-84, 2000
Metz TO, et al, Pyridoxamine traps intermediates in lipid peroxidation reactions in vivo: evidence on the role of lipids and chemical modification of protein and development of diabetic complications, J Biol Chem 278:42012-19, 2003
Booth AA, et al, Thiamine pyrophosphate and pyridoxamine inhibit the formation of antigenic advanced glycation endproducts: comparison with aminoguanidine, Biochem Biophys Res Commun, 220:113-19, 1996
Stitt A, et al, The AGE inhibitor pyridoxine and inhibits development of retinopathy in experimental diabetes, Diabetes 51:2826-32, 2000
Laines-Cessac P, et al, Mechanisms of the inhibition of human erythrocyte pyridoxal kinase by drugs, Biochem Pharmacol 54:863-70, 1997


The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the research and experience of Dr. Grisanti and his community. Dr. Grisanti encourages you to make your own health care decisions based upon your research and in partnership with a qualified health care professional.

You may have heard of a treatment called dry needling and wondered what exactly it is or if it’s something that may be right for you.
While the name of the procedure may sound intimidating, dry needling is safe, minimally discomforting and often an effective technique for patients with certain musculoskeletal presentations. Dry needling is a treatment performed by skilled, trained physical therapists, certified in the procedure. A thin monofilament needle penetrates the skin and treats underlying muscular trigger points for the management of neuromusculoskeletal pain and movement impairments.
So, what is a trigger point? A trigger point is a local contracture or tight band in a muscle fiber that can disrupt function, restrict range of motion, refer pain or cause local tenderness. When dry needling is applied to a dysfunctional muscle or trigger point, it can decrease banding or tightness, increase blood flow, and reduce local and referred pain.
It’s important to note dry needling is not the same as acupuncture. It uses similar tools, but that’s where the similarities end. Dry needling is performed by different practitioners with different training. Acupuncture is based on Eastern medicine, while dry needling is rooted in Western medicine and evaluation of pain patterns, posture, movement impairments, function and orthopedic tests.
Dry needling treats muscle tissue, and its goal is to reduce pain, inactivate trigger points and restore function. It rarely is a standalone procedure. Rather, it often is part of a broader physical therapy approach incorporating other traditional physical therapy interventions into treatment.
Dry needling can be used for a wide variety of musculoskeletal issues, such as shoulder, neck, heel, hip and back pain. While research indicates dry needling is a safe and effective approach for treating and managing pain, some insurance companies may not reimburse for the procedure.


Written by:
Kara Johnson, D.P.T. 
Physical Therapy 

​There is a silent epidemic of blindness which is gradually sweeping over aging Americans.

This common blindness is being caused by macular degeneration. Macular degeneration is now the #1 most common cause of blindness in adults. In fact, one in ten folks over age 60 has already unknowingly started the changes of early macular degeneration.

The macula is in the center of the retina (the layer of tissue on the inside back wall of your eyeball). It deteriorates in a variety of ways. There are two types of macular degeneration. One type is called dry macular degeneration which is more common and less severe. The other type is called wet macular degeneration. Wet macular degeneration is generally caused by abnormal blood vessels that leak fluid or blood into the region of the macula creating scar tissue while dry macular degeneration is a steady deterioration or rotting away of the back of the eyeball.
Considering the wealth of information on clinically documented cures for this disease it baffles me why so many ophthalmologists are clueless about the causes and cures of this eye disease. You wonder how a person who specializes in one tiny organ, the eyeball, can fail to want to know everything there is to know about it.
So what are the causes?
As people get older and get macular degeneration or other eye problems that their levels of two nutrient called lutein and zeaxanthin go down, as opposed to folks who keep healthful levels in their eyes. Lutein and zeaxanthin are carotenoids from our foods that are present in the highest concentration in the retina. No other place in the body is higher.
Spinach is a wonderful source of lutein and the most potent form in supplements I've found is 20 mg Lutein (also contains zeaxanthin). Is important to note that improvement deteriorated if they discontinued the supplements.
And of course eating a lot of dark green leafy vegetables and not just relying solely on nutrients has improved vision in 71% of participants.
It shocks me that with the most expensive and high-tech medical system on the planet, more ophthalmologists don't do the obvious and that is to check the nutritional status of their patients. Many folks have completely gotten rid of their macular degeneration.
But like anything else, the earlier it is attacked, the better the results.
The bottom line?
Take a daily Lutein 20 mg and anyone with any type of eye disease should get the Cardio/ION with an expert interpretation. Your whole future depends on your eyes. 
 
References:

• Richer S, et at, Double-masked, placebo-controlled, randomized trial of lutein and antioxidant supplementation in the intervention of atrophic age-related macular degeneration: the Veterans LAST Study (Lutein Antioxidant Supplementation Trial), Optometry 75:216-30, 2004
• Rogers Sherry, Total Wellness, Prestige Publishing, December 2010
• Ma L, Yan SF, Huang YM, Lu XR, Qian F, Pang HL, Xu XR, Zou ZY, Dong PC, Xiao X, Wang X, Sun TT, Dou HL, Lin XM. Effect of lutein and zeaxanthin on macular pigment and visual function in patients with early age-related macular degeneration. Ophthalmology. 2012 Nov;119(11):2290-7.
• Weigert G, Kaya S, Pemp B, Sacu S, Lasta M, Werkmeister RM, Dragostinoff N, Simader C, Garhöfer G, Schmidt-Erfurth U, Schmetterer L. Effects of lutein supplementation on macular pigment optical density and visual acuity in patients with age-related macular degeneration. Invest Ophthalmol Vis Sci. 2011 Oct 17;52
• Murray IJ, Makridaki M, van der Veen RL, Carden D, Parry NR, Berendschot TT. Lutein supplementation over a one-year period in early AMD might have a mild beneficial effect on visual acuity: the CLEAR study. Invest Ophthalmol Vis Sci. 2013 Mar 11;54(3)
• Carpentier S, Knaus M, Suh M. Associations between lutein, zeaxanthin, and age-related macular degeneration: an overview. Crit Rev Food Sci Nutr. 2009 Apr;49(4):313-26. Falsini B, et at, Influence of short-term antioxidant supplementation on macular function in age-related maculopathy: a pilot study including electrophysiologic assessment, Ophthalmology 110:51-61, 2003
• Richer S, ARMD-pilot (case series) and environmental intervention data, J Am Optom Assoc 70:24-6, 1999
• Gaby AR, Nutritional Medicine, Fritz Perlberg Publishing, Concord NH, 2011 Pelton R, et at, Drug-Induced Nutrients Completion Handbook, 2"d Ed, 1-877¬836-5394, 2001

Obesity has hit epidemic proportions and the world is desperate to do anything to lose their unwanted fat.

Although eating a healthy diet and exercise is paramount to losing fat, there is one little unknown fact that will prevent millions of people from ever losing fat.
According to the US government this one thing is the considered the number one pollutant in the human body and will put a quick halt to ever reaching your desired level of fitness and fat loss.
One of the major causes of the obesity epidemic is the unprecedented level of phthalates or plasticizers.

The problem with these toxic environmental toxins is the fact that they are difficult to impossible to avoid. In fact they are found in every species even in the most pristine wild.

In fact we have so damaged the chemistry of even animals in the wild that the polar bears in the Arctic have human diseases such as hypothyroidism and osteoporosis.

Phthalates are the highest pollutant in the body being over 10,000 times higher than any of the thousands of other environmental toxins.

In fact they are so pervasive that now children six years of age have levels that used to take adults until the age of 40 to accumulate.

Phthalates are the highest pollutant in the body being over 10,000 times higher than any of the thousands of other environmental toxins.

-The government agencies, scientific and medical literature have clearly documented that a huge amount of these environment toxins (phthalates) come from our water, soda and infant formula bottles, food packaging, cosmetics, nail polish, mattresses, couches, carpets, clothing, medications, styrofoam cups, IVs, vinyl flooring, construction materials, home wiring, computers, industrial and auto exhausts, etc.,

The sad point is the fact that these toxins stockpile in the body and overwhelm our ability to detoxify them.
We routinely measure them with a wonderful test called Phthalates & Parabens Profile (https://www.gdx.net/product/phthalates-parabens-test-urine)
In addition to the damage these environmental toxins do to the biochemistry of losing fat they have also been known to be associated with difficult to treat chronic fatigue syndrome,fibromyalgia, ADD,  syndrome X, diabetes, arteriosclerosis, allergies, and much more.
In fact the label that a disease has is now unimportant. All we care about is what caused the disease and what biochemical corrections are necessary to get rid of it and actually bring about a true solution, a word you rarely hear in drug-oriented medicine.
What is even worse is the fact a pregnant mother's phthalate levels (look at how many are continually drinking from plastic water bottles, etc., thinking that it's something healthful) hugely influence not only the development of the child's brain and glands, but even future fertility and cancers in their unborn children, not to mention, of course, obesity.
What you need to understand and something the researchers have forgot to mention is the fact that fat stores a huge amount of our chemicals, so the fatter you are the more the difficult it is to lose fat. Interesting and at the same time depressing.

The bottom line is many people will never lose weight or solve their medical problems because they have not gotten rid of the phthalates and other environmental pollutants that have damaged their chemistry and genetics.

One of the key ingredients to ridding the body of these harmful toxins is first to do what you can to avoid it (STOP DRINKING OUT OF SYROFORM CUPS and PLASTIC BOTTLES) and invest in a far infrared sauna

References:
Ronald Grisanti D.C., D.A.B.C.O., DACBN, MS, CFMP
​
Heindal JJ, Endocrine disruptors and the obesity epidemic, Toxicol Sci 76; 2:247-49, 2003

Baillie-Hamilton PF, Chemical toxins: a hypothesis to explain the global obesity epidemic, JAIt Complement Med 8;2:185-92, 2002

Alonso-Magdalena P, et al, The estrogenic effect of bisphenol A disrupts pancreatic B-cell function in vivo and induces insulin resistance, Environ Health Perspect 114:106-12, 2006

The Hundred Year Diet in the Wall Street (May 10, 2010, A I5)

Vom Saal FS, Welshons WV, Large effects from small exposures. II. The importance of positive controls in low-dose research on bisphenol A, Environ Res, 100;1:50-76, Jan. 2006

Feige JN, et al, The endocrine disruptor monoethyl-hexyl phthalate is a selective peroxisome proliferator-activated receptor gamma modulator that promotes adipogenesis, JBiol Chem 282:19152-66, 2007

Hatch EE, et al., Association of urinary phthalate metabolite concentrations with a body mass index and waist circumference: a cross-sectional study of NHANES data, 1999-2002, Environ Health 7:27, 2008

Clark K, et al, Observed concentrations in the environment. In: The Handbook of Environmental Chemistry. Vol 3, Part Q. Phthalate Ester (Staples CA, ed). New York: Springer, 125-177, 2003

Feige JN, et al, The pollutant diethylhexyl phthalate regulates hepatic energy metabolism via species-specific PPARa-dependent mechanisms, Environ Health Persp, 118; 2:234-41, Feb 2010

Jaakkola JJK, et al, The role of exposure to phthalates from polyvinyl chloride products in the development of asthma and allergies: A systematic review and meta-analysis, Environ Health Perspect 116:845-53, 2008

 
Before starting any self treatment Dr. Grisanti recommends that you consider consulting with a doctor trained in functional medicine.  
The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the research and experience of Dr. Grisanti and his functional medicine community. Dr. Grisanti encourages you to make your own health care decisions based upon your research and in partnership with a qualified health care professional. 

​A study published in Nature revealed that improving the gut microbiota could be a potential target in addressing Autism Spectrum Disorder (ASD).  While it is known that the gut microbiota impacts health in many ways, it seems that modulating gut bacteria may also help to mitigate autism symptoms.
In this study, the researchers re-evaluated a small group of 18 ASD children who had severe digestive issues. Two years prior, these children underwent Microbiota Transfer Therapy (MTT), which consisted of antibiotics, cleansing the bowels, suppressing stomach acid and a fecal microbiota transplant. At the time of the MTT, the results showed significant increases in bacterial diversity along with marked improvements in both gastrointestinal (GI) and ASD symptoms for participants. This follow-up study subsequently found that two years after the MTT, bacterial diversity persisted and both GI and ASD symptoms remained “improved” compared to baseline according to the same GI and behavioral tests that were utilized previously.
Currently, one in 59 children in America have ASD. A great majority of individuals with neurobehavioral disorders, such as ASD, also experience chronic gastrointestinal symptoms. Established research supports the notion that ASD children have distinct gut microbiomes compared to neurotypical children.
This novel study highlights a non-human microbial cell perspective of neurobehavioral health, one that could help to treat conditions like ASD. The need for microbiota therapy is exigent as the study points out that currently “no medical treatment has been approved to treat core symptoms of ASD, such as social communication difficulties and repetitive behaviors”.

Sleeping more on the weekend to recover from sleep lost during a busy workweek is very common. Yet, recent study findings suggest that sleeping more on the weekend is not an effective strategy, and still leads to metabolic dysregulation and a higher risk of metabolic problems such as obesity and diabetes.
The study examined the connection between habitual weekend “recovery sleeping” and circadian timing, energy intake, weight gain and insulin sensitivity. Healthy, young adults were used as study participants and were assigned to one of three groups. The first group was the control group and had 9-hour sleep opportunities. The second had sleep restriction without weekend recovery sleep and 5-hour sleep opportunities. The third group was allowed to sleep for 5 hours during a 5-day workweek, as well as 2 days of weekend recovery sleep, followed by 2 nights of insufficient sleep.
The results showed that insufficient sleep increased after-dinner energy intake, as well as body weight. During weekend recovery, the participants slept for 1.1 hours more than the baseline group, and after-dinner energy intake decreased once again. However, when the participants experienced insufficient sleep after the weekend, the after-dinner intake and body weight increased again. The group that had only insufficient sleep had decreased insulin sensitivity compared with baseline, and the drop was approximately 13%. Yet the insulin resistance of those who were allowed to recover at the weekend equally dropped by between 9 and 27%. Without management, insulin sensitivity can lead to further metabolic issues. 
This study suggests that sleeping more on the weekends to recover from a recurrent lack of sleep during the week is not as health-promoting as getting sustained good-quality sleep throughout the week.