Vitamin D Deficiency Associated With Chronic Fatigue in Brain Injured Patients

New evidence presented at the European Congress of Endocrinology has shown that vitamin D deficiency is closely associated with the chronic fatigue that often follows post traumatic brain injury (TBI).

TBI is a major cause of death and disability worldwide. In the European Union the annual incidence of TBI hospitalizations and fatalities is estimated at 235 per 100,000 people. This means that on average a large European state such as the UK, France or Germany, will have around 140,000 new traumatic brain injuries every year (national figures vary). Around two-thirds of post TBI patients go on to suffer chronic fatigue. Now a group of researchers in the Netherlands have linked vitamin D deficiency to chronic fatigue in post-TBI sufferers.

The group, led by Dr Jessica Schnieders from Rijnstate Hospital in Arnham, The Netherlands, looked at vitamin D and hormone levels in 90 fatigued and non-fatigued subjects. They also systematically evaluated pituitary hormones and factors such as sleep, attention, emotional well-being, quality of life, coping style, and daily activity. They found that 51% of TBI patients were severely fatigued 10 years after the trauma. Vitamin D deficiency was present in 65% of post TBI patients and significantly related with fatigue (P<0.05), with patients who suffered from fatigue more likely to be vitamin D deficient. The group also found a higher incidence of growth hormone and sex hormone deficiency in the fatigued group, but they found no evidence that these deficiencies contributed to the fatigue.

This work opens the possibility that correcting the vitamin D deficiency might help to reduce some of the chronic fatigue in TBI patients. However, as vitamin D levels in the body are affected by diet and time spent in the sunshine, further studies are now needed to confirm whether low vitamin D levels are a cause of the fatigue or whether they are a consequence of altered lifestyle led due to suffering from fatigue.

Lead researcher, Dr Jessica Schnieders said: "In the Netherlands we have 30,000 people every year who suffer a traumatic brain injury and many of these go on to suffer from chronic fatigue. This is early work, so we need to confirm that vitamin D is the cause of this fatigue, and if so to see if taking vitamin D, perhaps coupled with improved sleep patterns, can alleviate some of the symptoms.

"We looked at patients around 10 years after their trauma. Fatigued post traumatic brain injury patients are less active, and generally experience a reduced quality of life. They have difficulties in maintaining relationships and keeping jobs, and are less independent than people who have not had to cope with such trauma."

New evidence presented at the European Congress of Endocrinology has shown that vitamin D deficiency is closely associated with the chronic fatigue that often follows post traumatic brain injury (TBI).

TBI is a major cause of death and disability worldwide. In the European Union the annual incidence of TBI hospitalizations and fatalities is estimated at 235 per 100,000 people. This means that on average a large European state such as the UK, France or Germany, will have around 140,000 new traumatic brain injuries every year (national figures vary). Around two-thirds of post TBI patients go on to suffer chronic fatigue. Now a group of researchers in the Netherlands have linked vitamin D deficiency to chronic fatigue in post-TBI sufferers.

The group, led by Dr Jessica Schnieders from Rijnstate Hospital in Arnham, The Netherlands, looked at vitamin D and hormone levels in 90 fatigued and non-fatigued subjects. They also systematically evaluated pituitary hormones and factors such as sleep, attention, emotional well-being, quality of life, coping style, and daily activity. They found that 51% of TBI patients were severely fatigued 10 years after the trauma. Vitamin D deficiency was present in 65% of post TBI patients and significantly related with fatigue (P<0.05), with patients who suffered from fatigue more likely to be vitamin D deficient. The group also found a higher incidence of growth hormone and sex hormone deficiency in the fatigued group, but they found no evidence that these deficiencies contributed to the fatigue.

This work opens the possibility that correcting the vitamin D deficiency might help to reduce some of the chronic fatigue in TBI patients. However, as vitamin D levels in the body are affected by diet and time spent in the sunshine, further studies are now needed to confirm whether low vitamin D levels are a cause of the fatigue or whether they are a consequence of altered lifestyle led due to suffering from fatigue.

Lead researcher, Dr Jessica Schnieders said: "In the Netherlands we have 30,000 people every year who suffer a traumatic brain injury and many of these go on to suffer from chronic fatigue. This is early work, so we need to confirm that vitamin D is the cause of this fatigue, and if so to see if taking vitamin D, perhaps coupled with improved sleep patterns, can alleviate some of the symptoms.

"We looked at patients around 10 years after their trauma. Fatigued post traumatic brain injury patients are less active, and generally experience a reduced quality of life. They have difficulties in maintaining relationships and keeping jobs, and are less independent than people who have not had to cope with such trauma."

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'Epigenetic' concepts offer new approach to degenerative disease

ANAHEIM, Calif. – In studies on cancer, heart disease, neurological disorders and other degenerative conditions, some scientists are moving away from the "nature-versus-nurture" debate and are finding you're not a creature of either genetics or environment, but both – with enormous implications for a new approach to health.

The new field of "epigenetics" is rapidly revealing how people, plants and animals do start with a certain genetic code at conception. But the choice of which genes are "expressed," or activated, is strongly affected by environmental influences. The expression of genes can change rapidly over time, they can be influenced by external factors, those changes can be passed along to offspring, and they can literally hold the key to life and death.

Some of the newest work in this field was outlined today by researchers from the Linus Pauling Institute at Oregon State University, speaking at Experimental Biology 2010, a professional conference in Anaheim, Calif.

According to Rod Dashwood, a professor of environmental and molecular toxicology and head of LPI's Cancer Chemoprotection Program, epigenetics is a unifying theory in which many health problems, ranging from cancer to cardiovascular disease and neurological disorders, can all be caused at least in part by altered "histone modifications," and their effects on the reading of DNA in cells.

"We believe that many diseases that have aberrant gene expression at their root can be linked to how DNA is packaged, and the actions of enzymes such as histone deacetylases, or HDACs," Dashwood said. "As recently as 10 years ago we knew almost nothing about HDAC dysregulation in cancer or other diseases, but it's now one of the most promising areas of health-related research."

In the case of cancer, tumor suppressor genes can cause cancer cells to die by acting as a brake on unrestrained cell growth. But too much of the HDAC enzyme can "switch off" tumor suppressor genes, even though the underlying DNA sequence of the cell – its genetic structure – has not been changed or mutated. If this happens, cells continue to replicate without restraint, which is a fundamental characteristic of cancer development.

The good news – for cancer and perhaps many other health problems – is that "HDAC inhibitors" can stop this degenerative process, and some of them have already been identified in common foods. Examples include sulforaphane in broccoli, indole-3-carbinol in cruciferous vegetables, and organosulfur compounds in vegetables like garlic and onions. Butyrate, a compound produced in the intestine when dietary fiber is fermented, is an HDAC inhibitor, and it provides one possible explanation for why higher intake of dietary fiber might help prevent cancer.

"Metabolism seems to be a key factor, too, generating the active HDAC inhibitor at the site of action," Dashwood said. "In cancer cells, tumor suppressors such as p21 and p53 often become epigenetically silenced. HDAC inhibitors can help turn them on again, and trick the cancer cell into committing suicide via apoptosis.

"We already know some of the things people can do to help prevent cancer with certain dietary or lifestyle approaches," Dashwood said. "Now we're hoping to more fully understand the molecular processes going on, including at the epigenetic level. This should open the door for new approaches to disease prevention or treatment through diet, as well as in complementing conventional drug therapies."

OSU scientists recently received an $8.5 million grant from the National Cancer Institute to explore these issues, making the LPI program one of the leaders in the nation on diet, epigenetics, and cancer prevention. The positive findings of laboratory research are already being converted to placebo-controlled human intervention trials on such health concerns as colon and prostate cancer, which are among the most common cancers in the United States.

OSU scientists have published a number of studies on these topics in professional journals such as Cancer Research, Cancer Prevention Research, Carcinogenesis, and Seminars in Cancer Biology. Among the most recent findings is that naturally occurring organoselenium compounds in the diet might prevent the progress of human prostate and colon cancer through an HDAC inhibition mechanism.

"Some therapeutic drugs already used for cancer treatment in the clinical setting probably work, at least in part, because they are acting as HDAC inhibitors," Dashwood said. "And what's most intriguing is that HDAC inhibition may affect many degenerative health issues, not just cancer. Heart disease, stroke, bipolar disorder, and even aging may all have links to HDAC/histone alterations.

"In the future, a single HDAC inhibitor conceptually could have benefits for more than one degenerative disease problem."

ANAHEIM, Calif. – In studies on cancer, heart disease, neurological disorders and other degenerative conditions, some scientists are moving away from the "nature-versus-nurture" debate and are finding you're not a creature of either genetics or environment, but both – with enormous implications for a new approach to health.

The new field of "epigenetics" is rapidly revealing how people, plants and animals do start with a certain genetic code at conception. But the choice of which genes are "expressed," or activated, is strongly affected by environmental influences. The expression of genes can change rapidly over time, they can be influenced by external factors, those changes can be passed along to offspring, and they can literally hold the key to life and death.

Some of the newest work in this field was outlined today by researchers from the Linus Pauling Institute at Oregon State University, speaking at Experimental Biology 2010, a professional conference in Anaheim, Calif.

According to Rod Dashwood, a professor of environmental and molecular toxicology and head of LPI's Cancer Chemoprotection Program, epigenetics is a unifying theory in which many health problems, ranging from cancer to cardiovascular disease and neurological disorders, can all be caused at least in part by altered "histone modifications," and their effects on the reading of DNA in cells.

"We believe that many diseases that have aberrant gene expression at their root can be linked to how DNA is packaged, and the actions of enzymes such as histone deacetylases, or HDACs," Dashwood said. "As recently as 10 years ago we knew almost nothing about HDAC dysregulation in cancer or other diseases, but it's now one of the most promising areas of health-related research."

In the case of cancer, tumor suppressor genes can cause cancer cells to die by acting as a brake on unrestrained cell growth. But too much of the HDAC enzyme can "switch off" tumor suppressor genes, even though the underlying DNA sequence of the cell – its genetic structure – has not been changed or mutated. If this happens, cells continue to replicate without restraint, which is a fundamental characteristic of cancer development.

The good news – for cancer and perhaps many other health problems – is that "HDAC inhibitors" can stop this degenerative process, and some of them have already been identified in common foods. Examples include sulforaphane in broccoli, indole-3-carbinol in cruciferous vegetables, and organosulfur compounds in vegetables like garlic and onions. Butyrate, a compound produced in the intestine when dietary fiber is fermented, is an HDAC inhibitor, and it provides one possible explanation for why higher intake of dietary fiber might help prevent cancer.

"Metabolism seems to be a key factor, too, generating the active HDAC inhibitor at the site of action," Dashwood said. "In cancer cells, tumor suppressors such as p21 and p53 often become epigenetically silenced. HDAC inhibitors can help turn them on again, and trick the cancer cell into committing suicide via apoptosis.

"We already know some of the things people can do to help prevent cancer with certain dietary or lifestyle approaches," Dashwood said. "Now we're hoping to more fully understand the molecular processes going on, including at the epigenetic level. This should open the door for new approaches to disease prevention or treatment through diet, as well as in complementing conventional drug therapies."

OSU scientists recently received an $8.5 million grant from the National Cancer Institute to explore these issues, making the LPI program one of the leaders in the nation on diet, epigenetics, and cancer prevention. The positive findings of laboratory research are already being converted to placebo-controlled human intervention trials on such health concerns as colon and prostate cancer, which are among the most common cancers in the United States.

OSU scientists have published a number of studies on these topics in professional journals such as Cancer Research, Cancer Prevention Research, Carcinogenesis, and Seminars in Cancer Biology. Among the most recent findings is that naturally occurring organoselenium compounds in the diet might prevent the progress of human prostate and colon cancer through an HDAC inhibition mechanism.

"Some therapeutic drugs already used for cancer treatment in the clinical setting probably work, at least in part, because they are acting as HDAC inhibitors," Dashwood said. "And what's most intriguing is that HDAC inhibition may affect many degenerative health issues, not just cancer. Heart disease, stroke, bipolar disorder, and even aging may all have links to HDAC/histone alterations.

"In the future, a single HDAC inhibitor conceptually could have benefits for more than one degenerative disease problem."

Read More

Rickettsial Organisms in Cats in the West Indies

Kelly PJ, Lucas H, Eremeeva ME, Dirks KG, Rolain JM, Yowell C, Thomas R, Douglas T, Dasch GA, Raoult D. Rickettsia felis, West Indies. Emerg Infect Dis. 2010 Mar;16(3):570-1.

A study examining levels of antibody to the spotted fever group of Rickettsial organisms in feral cats from a spay/neuter program on St. Kitts found that most (45/68) were seropositive for this group of bacteria. These bacteria are transmitted by ticks, and have been associated with disease in some animals. Interestingly, no ticks were found on any of the cats, but they were infested with fleas. Fleas are known to be the vector for one rickettsial organism, Rickettsia felis. This bacterium is not harmful to cats, but can cause spotted fever in humans. These investigators also looked for the organism itself in cat fleas, and found the organism in about 20% of the fleas they tested. This was the first identification of this organism in the Caribbean, and indicates cats may be sentinels for its presence in a particular locale. [MK]

Related articles:
Hawley JR, Shaw SE, Lappin MR: Prevalence of Rickettsia felis DNA in the blood of cats and their fleas in the United States, J Feline Med Surg 9:258, 2007.

Bayliss DB, Morris AK, Horta MC et al: Prevalence of Rickettsia species antibodies and Rickettsia species DNA in the blood of cats with and without fever, J Feline Med Surg 11:266, 2009.

More on cat health: Winn Feline Foundation Library
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Kelly PJ, Lucas H, Eremeeva ME, Dirks KG, Rolain JM, Yowell C, Thomas R, Douglas T, Dasch GA, Raoult D. Rickettsia felis, West Indies. Emerg Infect Dis. 2010 Mar;16(3):570-1.

A study examining levels of antibody to the spotted fever group of Rickettsial organisms in feral cats from a spay/neuter program on St. Kitts found that most (45/68) were seropositive for this group of bacteria. These bacteria are transmitted by ticks, and have been associated with disease in some animals. Interestingly, no ticks were found on any of the cats, but they were infested with fleas. Fleas are known to be the vector for one rickettsial organism, Rickettsia felis. This bacterium is not harmful to cats, but can cause spotted fever in humans. These investigators also looked for the organism itself in cat fleas, and found the organism in about 20% of the fleas they tested. This was the first identification of this organism in the Caribbean, and indicates cats may be sentinels for its presence in a particular locale. [MK]

Related articles:
Hawley JR, Shaw SE, Lappin MR: Prevalence of Rickettsia felis DNA in the blood of cats and their fleas in the United States, J Feline Med Surg 9:258, 2007.

Bayliss DB, Morris AK, Horta MC et al: Prevalence of Rickettsia species antibodies and Rickettsia species DNA in the blood of cats with and without fever, J Feline Med Surg 11:266, 2009.

More on cat health: Winn Feline Foundation Library
Join us on Facebook
Follow us on Twitter

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Study finds green tea could reduce glaucoma risk

Green tea catechins could help protect against glaucoma and other eye diseases, according to a new research which found that the ingredients travel from the digestive system into the tissues of the eyes.

The results of the study from researchers based at the Chinese University of Hong Kong and the Hong Kong Eye Hospital were published in the Journal of Agricultural and Food Chemistry and indicate that green tea consumption could benefit the eye against oxidative stress.

The scientists analyzed eye tissue from rats that drank green tea and found that the lens, retina and other tissues absorbed significant amounts of green tea catechins.

Although many antioxidants have been studied in the eye, the authors claim that theirs is the first paper to show distribution of individual catechins after ingestion of green tea extract and to evaluate their in vivo antioxidative effects in various parts of the eye.

The authors said that oxidative stress causes biological disturbances such as DNA damage and activation of proteolytic enzymes that can lead to tissue cell damage or dysfunction and eventually many ophthalmic diseases.

“Photooxidative stress can inactivate catalase in the lens to initiate cataract formation, while long-term effects of reactive oxygen intermediates could damage retinal tissue cells retinal pigment epithelium, and choriocapillaries . Oxidation is also associated with primary open angle glaucoma (POAG),” they said.

Green tea benefits

Other reported benefits for green tea have been risk reduction in terms of educing the risk of Alzheimer's and certain cancers, improving cardiovascular and oral health, as well as aiding in weight management.

Green tea contains between 30 and 40 per cent of water-extractable polyphenols, and the four primary polyphenols found in fresh tealeaves are epigallocatechin gallate (EGCG), epigallocatechin (EGC), epicatechin gallate ECG), and epicatechin (EC).

The success has translated into a booming extract market, valued at a around $44m (€29.7m), according to recent report from Frost & Sullivan, and they predict the market is will grow by more than 13 per cent over the next seven years.
The study

Green tea extract (GTE) in tablet form was suspended in 0.5 mL of water, said the authors.

A dosage of 550 mg/kg of GTE was fed to the rats and the authors added that the doses of catechins were comparable to most published reports: 178 mg/kg epigallocatechin gallate - EGCG, 82.7 mg/kg, epicatechin gallate - ECG, 80.7 mg/kg gallocatechin gallate - GCG, 72.0 mg/kg epicatechin - EC, 58.7 mg/kg epigallocatechin - EGC, 56.7 mg/kg gallocatechin - GC, and 24 mg/kg catechin - C.

The rats, said the researchers, were sacrificed at different time intervals. And the eyes of the animals were then dissected into cornea, lens, retina, choroid-sclera, vitreous humor, and aqueous humor for analysis of catechins and 8-epi-isoprostane by HPLC-ECD and GC-NCI-MS, respectively.

Analysis of eye tissues demonstrated that eye structures absorbed significant amounts of individual catechins, said the researchers.

And the time of maximum concentration of the catechins varied from 30 minutes to around 12 hours, they continued.

The authors found that catechins were differentially distributed in eye tissues - the retina absorbed the highest levels of gallocatechin, while the aqueous humor tended to absorb epigallocatechin.

Significant reductions in 8-epi-isoprostane levels were found in the compartments except the choroid-sclera or plasma, indicating antioxidative activities of catechins in these tissues, concluded the team.

Green tea catechins could help protect against glaucoma and other eye diseases, according to a new research which found that the ingredients travel from the digestive system into the tissues of the eyes.

The results of the study from researchers based at the Chinese University of Hong Kong and the Hong Kong Eye Hospital were published in the Journal of Agricultural and Food Chemistry and indicate that green tea consumption could benefit the eye against oxidative stress.

The scientists analyzed eye tissue from rats that drank green tea and found that the lens, retina and other tissues absorbed significant amounts of green tea catechins.

Although many antioxidants have been studied in the eye, the authors claim that theirs is the first paper to show distribution of individual catechins after ingestion of green tea extract and to evaluate their in vivo antioxidative effects in various parts of the eye.

The authors said that oxidative stress causes biological disturbances such as DNA damage and activation of proteolytic enzymes that can lead to tissue cell damage or dysfunction and eventually many ophthalmic diseases.

“Photooxidative stress can inactivate catalase in the lens to initiate cataract formation, while long-term effects of reactive oxygen intermediates could damage retinal tissue cells retinal pigment epithelium, and choriocapillaries . Oxidation is also associated with primary open angle glaucoma (POAG),” they said.

Green tea benefits

Other reported benefits for green tea have been risk reduction in terms of educing the risk of Alzheimer's and certain cancers, improving cardiovascular and oral health, as well as aiding in weight management.

Green tea contains between 30 and 40 per cent of water-extractable polyphenols, and the four primary polyphenols found in fresh tealeaves are epigallocatechin gallate (EGCG), epigallocatechin (EGC), epicatechin gallate ECG), and epicatechin (EC).

The success has translated into a booming extract market, valued at a around $44m (€29.7m), according to recent report from Frost & Sullivan, and they predict the market is will grow by more than 13 per cent over the next seven years.
The study

Green tea extract (GTE) in tablet form was suspended in 0.5 mL of water, said the authors.

A dosage of 550 mg/kg of GTE was fed to the rats and the authors added that the doses of catechins were comparable to most published reports: 178 mg/kg epigallocatechin gallate - EGCG, 82.7 mg/kg, epicatechin gallate - ECG, 80.7 mg/kg gallocatechin gallate - GCG, 72.0 mg/kg epicatechin - EC, 58.7 mg/kg epigallocatechin - EGC, 56.7 mg/kg gallocatechin - GC, and 24 mg/kg catechin - C.

The rats, said the researchers, were sacrificed at different time intervals. And the eyes of the animals were then dissected into cornea, lens, retina, choroid-sclera, vitreous humor, and aqueous humor for analysis of catechins and 8-epi-isoprostane by HPLC-ECD and GC-NCI-MS, respectively.

Analysis of eye tissues demonstrated that eye structures absorbed significant amounts of individual catechins, said the researchers.

And the time of maximum concentration of the catechins varied from 30 minutes to around 12 hours, they continued.

The authors found that catechins were differentially distributed in eye tissues - the retina absorbed the highest levels of gallocatechin, while the aqueous humor tended to absorb epigallocatechin.

Significant reductions in 8-epi-isoprostane levels were found in the compartments except the choroid-sclera or plasma, indicating antioxidative activities of catechins in these tissues, concluded the team.

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The Claim: Lack of Sleep Increases Weight

Looking to lose a little weight? Portion size and exercise are crucial. But don’t forget about a good night’s rest.

Scientists have known for years that skimping on sleep is associated with weight gain. A good example was a study published in 2005, which looked at 8,000 adults over several years as part of the National Health and Nutrition Examination Survey. Sleeping fewer than seven hours a night corresponded with a greater risk of weight gain and obesity, and the risk increased for every hour of lost sleep.

More recent studies have taken a much closer look.

One published this year in The American Journal of Clinical Nutrition took a small group of men and measured their food intake across two 48-hour periods, one in which they slept eight hours and another in which they slept only four. After the night of abbreviated sleep, the men consumed more than 500 extra calories (roughly 22 percent more) than they did after eight hours of sleep. A University of Chicago study last year had similar findings in both men and women: subjects took in significantly more calories from snacks and carbohydrates after five and a half hours of sleep than after eight and a half hours.

Some studies pin the blame on hormones, arguing that decreased sleep creates a spike in ghrelin, a hormone that stimulates appetite, and a reduction in leptin, which signals satiety. But more study is needed.

THE BOTTOM LINE

Losing sleep may increase appetite and, as a result, weight.

Looking to lose a little weight? Portion size and exercise are crucial. But don’t forget about a good night’s rest.

Scientists have known for years that skimping on sleep is associated with weight gain. A good example was a study published in 2005, which looked at 8,000 adults over several years as part of the National Health and Nutrition Examination Survey. Sleeping fewer than seven hours a night corresponded with a greater risk of weight gain and obesity, and the risk increased for every hour of lost sleep.

More recent studies have taken a much closer look.

One published this year in The American Journal of Clinical Nutrition took a small group of men and measured their food intake across two 48-hour periods, one in which they slept eight hours and another in which they slept only four. After the night of abbreviated sleep, the men consumed more than 500 extra calories (roughly 22 percent more) than they did after eight hours of sleep. A University of Chicago study last year had similar findings in both men and women: subjects took in significantly more calories from snacks and carbohydrates after five and a half hours of sleep than after eight and a half hours.

Some studies pin the blame on hormones, arguing that decreased sleep creates a spike in ghrelin, a hormone that stimulates appetite, and a reduction in leptin, which signals satiety. But more study is needed.

THE BOTTOM LINE

Losing sleep may increase appetite and, as a result, weight.

Read More

Laughter Affects Body Like Exercise

Quite possibly. While toning thighs and building muscle mass still require a trip to the gym, other benefits associated with exercise — improved cholesterol and blood pressure, decreased stress hormones, a strengthened immune system and a healthy appetite — can be attained with regular guffaws, studies now suggest.

The latest mirth study, which focuses on the appetite effects of a good laugh, is being presented this week at the 2010 Experimental Biology conference in Anaheim, Calif.

Researchers measured the hormone levels of 14 volunteers before and after they watched a distressing or hilarious video clip. The researchers were particularly interested in two hormones known to regulate appetite: ghrelin, which spurs hunger, and leptin, which cues satiety.

The appetite hormones did not change significantly as people watched the upsetting video (the first 20 minutes of "Saving Private Ryan.")

But after the amusing video clip — either of stand-up comedians or a funny film — hormone levels changed as if the participant had engaged in moderate physical exercise. Specifically, ghrelin levels rose and leptin levels fell, indicating a possible increase in appetite. The lower leptin levels would mean the body isn't getting the "I'm full" message.

Overall, the finding adds to the understanding "that the body's response to repetitive laughter is similar to the effect of repetitive exercise," said study researcher Lee Berk of Loma Linda University in California in a press statement.

Although changes in appetite were not directly assessed, by, say, recording what people ate, the finding could help doctors treat patients who are suffering from loss of appetite but are too ill to exercise, explained Berk.

"It may indeed be true that laughter is good medicine," he said.

Quite possibly. While toning thighs and building muscle mass still require a trip to the gym, other benefits associated with exercise — improved cholesterol and blood pressure, decreased stress hormones, a strengthened immune system and a healthy appetite — can be attained with regular guffaws, studies now suggest.

The latest mirth study, which focuses on the appetite effects of a good laugh, is being presented this week at the 2010 Experimental Biology conference in Anaheim, Calif.

Researchers measured the hormone levels of 14 volunteers before and after they watched a distressing or hilarious video clip. The researchers were particularly interested in two hormones known to regulate appetite: ghrelin, which spurs hunger, and leptin, which cues satiety.

The appetite hormones did not change significantly as people watched the upsetting video (the first 20 minutes of "Saving Private Ryan.")

But after the amusing video clip — either of stand-up comedians or a funny film — hormone levels changed as if the participant had engaged in moderate physical exercise. Specifically, ghrelin levels rose and leptin levels fell, indicating a possible increase in appetite. The lower leptin levels would mean the body isn't getting the "I'm full" message.

Overall, the finding adds to the understanding "that the body's response to repetitive laughter is similar to the effect of repetitive exercise," said study researcher Lee Berk of Loma Linda University in California in a press statement.

Although changes in appetite were not directly assessed, by, say, recording what people ate, the finding could help doctors treat patients who are suffering from loss of appetite but are too ill to exercise, explained Berk.

"It may indeed be true that laughter is good medicine," he said.

Read More