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Phaceolus vulgaris

Botanical Name: Phaceolus vulgaris
Family:    Fabaceae
Subfamily:Faboideae
Tribe:    Phaseoleae
Subtribe:    Phaseolinae
Genus:    Phaseolus
Species:    P. vulgaris
Kingdom:    Plantae
Order:    Fabales

Common Names:Common bean,Kidney bean, String bean, Field bean, Flageolet bean, French bean, Garden bean, Haricot bean, Pop bean, or Snap bean

Habitat:Phaceolus vulgaris is  native of Indies; cultivated all over Europe; also said to be found in ancient tombs in Peru.

Description:
Phaceolus vulgaris is a herbaceous annual plant grown worldwide for its edible dry seed or unripe fruit that are both known as “beans”. The common bean is a highly variable species with a long history. Bush varieties form erect bushes 20–60 cm (8–20 in) tall, while pole or running varieties form vines 2–3 m (7–10 ft) long. All varieties bear alternate, green or purple leaves, which are divided into three oval, smooth-edged leaflets, each 6–15 cm (2–6 in) long and 3–11 cm (1–4 in) wide. The white, pink, or purple flowers are about 1 cm long, and they give way to pods 8–20 cm (3–8 in) long and 1–1.5 cm wide. These may be green, yellow, black, or purple in color, each containing 4–6 beans. The beans are smooth, plump, kidney-shaped, up to 1.5 cm long, range widely in color, and are often mottled in two or more colors. The wild P. vulgaris was native to the Americas and was domesticated separately in Mesoamerica and in the southern Andes region, giving the domesticated bean two gene pools which remain separate to this day.  Along with squash and maize (corn), beans are one of the “Three Sisters” central to indigenous North American agriculture…...CLICK & SEE THE PICTURES

Edible Uses:
Dry beans:
Similar to other beans, the common bean is high in starch, protein, and dietary fiber, and is an excellent source of iron, potassium, selenium, molybdenum, thiamine, vitamin B6, and folate.

Dry beans will keep indefinitely if stored in a cool, dry place, but as time passes, their nutritive value and flavor degrade and cooking times lengthen. Dried beans are almost always cooked by boiling, often after being soaked in water for several hours. While the soaking is not strictly necessary, it shortens cooking time and results in more evenly textured beans. In addition, soaking beans removes 5 to 10% of the gas-producing sugars that can cause flatulence for some people. The methods include simple overnight soaking and the power soak method in which beans are boiled for three minutes and then set aside for 2–4 hours. Before cooking, the soaking water is drained off and discarded. Dry common beans take longer to cook than most pulses: cooking times vary from one to four hours, but are substantially reduced with pressure cooking.

In Mexico, Central America, and South America, the traditional spice used with beans is epazote, which is also said to aid digestion. In East Asia, a type of seaweed, kombu, is added to beans as they cook for the same purpose. Salt, sugar, and acidic foods such as tomatoes may harden uncooked beans, resulting in seasoned beans at the expense of slightly longer cooking times.

Dry beans may also be bought cooked and canned as refried beans, or whole with water, salt, and sometimes sugar.

Its leaf is also occasionally used as a vegetable and the straw as fodder. Its botanical classification, along with other Phaseolus species, is as a member of the legume family Fabaceae, most of whose members acquire the nitrogen they require through an association with rhizobia, a species of nitrogen-fixing bacteria.

The common bean is a highly variable species that has a long history of cultivation. All wild members of the species have a climbing habit, but many cultivars are classified as “bush beans” or “pole beans”, depending on their style of growth. These include the kidney bean, the navy bean, the pinto bean, and the wax bean. The other major types of commercially grown bean are the runner bean (Phaseolus coccineus) and the broad bean (Vicia faba).

Beans are grown in every continent except Antarctica. Brazil and India are the largest producers of dry beans, while China produces, by far, the largest quantity of green beans. Worldwide, 23 million tonnes of dry common beans and 17.1 million tonnes of green beans were grown in 2010.

Cultivation:     
Requires a warm sunny position in a rich well-drained preferably light soil with plenty of moisture in the growing season[27, 37, 200]. Dislikes heavy, wet or acid soils[16, 37]. Prefers a pH in the range 5.5 to 6.5[200]. The French bean is commonly cultivated in the temperate and subtropical zones and in montane valleys of the tropics for its edible mature seeds and immature seedpods. It is often grown to provide a major part of the protein requirement[183, 269]. A very variable plant, there are more than 1,000 named varieties ranging from dwarf forms about 30cm tall to climbing forms up to 3 metres tall[183, 186, 200, 269]. Plants are not frost-tolerant, air temperatures below 10°c can cause damage to seedlings[200]. When grown for their edible pods, the immature pods should be harvested regularly in order to promote extra flower production and therefore higher yields[200]. Yields of green pods averages about 3kg per square metre, though double this can be achieved[200]. French beans grow well with strawberries, carrots, cauliflowers, cucumbers, cabbage, beet, leek and celeriac[18, 20]. They are inhibited by alliums and fennel growing nearby[18, 20]. This species has a symbiotic relationship with certain soil bacteria, these bacteria form nodules on the roots and fix atmospheric nitrogen. Some of this nitrogen is utilized by the growing plant but some can also be used by other plants growing nearby[200]. When removing plant remains at the end of the growing season, it is best to only remove the aerial parts of the plant, leaving the roots in the ground to decay and release their nitrogen.

Propagation:  
Pre-soak the seed for 12 hours in warm water and sow in mid spring in a greenhouse. Germination should take place within 10 days. When they are large enough to handle, prick the seedlings out into individual pots and plant them out after the last expected frosts. The seed can also be sown in situ in late spring though it may not ripen its seed in a cool summe

Constituents:  Starch and starchy fibrous matter, phaseoline, extractive albumen mucilage, pectic acid, legumin fatty matter, earthy salts, uncrystallizable sugar, inosite, sulphur

Medicinal  Uses:
Cancer;  Diuretic;  Homeopathy;  Hypoglycaemic;  Hypotensive;  Miscellany;  Narcotic.

The green pods are mildly diuretic and contain a substance that reduces the blood sugar level. The dried mature pod is used according to another report. It is used in the treatment of diabetes. The seed is diuretic, hypoglycaemic and hypotensive. Ground into a flour, it is used externally in the treatment of ulcers. The seed is also used in the treatment of cancer of the blood. When bruised and boiled with garlic they have cured intractable coughs. The root is dangerously narcotic. A homeopathic remedy is made from the entire fresh herb. It is used in the treatment of rheumatism and arthritis, plus disorders of the urinary tract.

When bruised and boiled with garlic Beans have cured otherwise uncurable coughs. If eaten raw they cause painful severe frontal headache, soreness and itching of the eyeball and pains in the epigastrium. The roots are dangerously narcotic.

Other Uses:
Biomass;  Dye;  Fungicide;  Miscellany.

A brown dye is obtained from red kidney beans. The plant contains phaseolin, which has fungicidal activity. Water from the cooked beans is very effective in reviving woollen fabrics. The plant residue remaining after harvesting the dried beans is a source of biomass.

Bean leaves have been used to trap bedbugs in houses. Microscopic hairs (trichomes) on the bean leaves entrap the insects. From ancient times, beans were used as device in various methods of divination. Fortune-telling using beans is called favomancy.

Known Hazards:     Large quantities of the raw mature seed are poisonous. Children eating just a few seeds have shown mild forms of poisoning with nausea and diarrhoea, though complete recovery took place in 12 – 24 hours. The toxins play a role in protecting the plant from insect predation.

Resources:
https://en.wikipedia.org/wiki/Phaseolus_vulgaris
http://www.pfaf.org/user/plant.aspx?LatinName=Phaseolus+vulgaris
http://www.botanical.com/botanical/mgmh/b/beakid21.html

Huntington’s Disease

Definition:
Huntington’s disease (also referred to in more formal medical research as Huntington Disease) is an hereditary neurological disorder of the central nervous system that causes progressive degeneration of cells in the brain, slowly impairing a person’s ability to walk, think, talk and reason.

Most people with Huntington’s disease develop signs and symptoms in their 40s or 50s, but the onset of disease may be earlier or later in life. When disease onset begins before age 20, the condition is called juvenile Huntington’s disease. Earlier onset often results in a somewhat different presentation of symptoms and faster disease progression.

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Medications are available to help manage the symptoms of Huntington’s disease, but treatments can’t prevent the physical, mental and behavioral decline associated with the condition.

It was first described in 1872 by an American doctor, George Huntington, who studied an extended family in Long Island affected by the condition.

Symptoms:
Symptoms of Huntington’s disease commonly become noticeable between the ages of 35 and 44 years, but they can begin at any age from infancy to old age. In the early stages, there are subtle changes in personality, cognition, and physical skills. The physical symptoms are usually the first to be noticed, as cognitive and psychiatric symptoms are generally not severe enough to be recognized on their own at the earlier stages. Almost everyone with Huntington’s disease eventually exhibits similar physical symptoms, but the onset, progression and extent of cognitive and psychiatric symptoms vary significantly between individuals.

The most characteristic initial physical symptoms are jerky, random, and uncontrollable movements called chorea. Chorea may be initially exhibited as general restlessness, small unintentionally initiated or uncompleted motions, lack of coordination, or slowed saccadic eye movements. These minor motor abnormalities usually precede more obvious signs of motor dysfunction by at least three years. The clear appearance of symptoms such as rigidity, writhing motions or abnormal posturing appear as the disorder progresses. These are signs that the system in the brain that is responsible for movement is affected.[6] Psychomotor functions become increasingly impaired, such that any action that requires muscle control is affected. Common consequences are physical instability, abnormal facial expression, and difficulties chewing, swallowing and speaking. Eating difficulties commonly cause weight loss and may lead to malnutrition.  Sleep disturbances are also associated symptoms. Juvenile HD differs from these symptoms in that it generally progresses faster and chorea is exhibited briefly, if at all, with rigidity being the dominant symptom. Seizures are also a common symptom of this form of HD.

Cognitive abilities are impaired progressively. Especially affected are executive functions which include planning, cognitive flexibility, abstract thinking, rule acquisition, initiating appropriate actions and inhibiting inappropriate actions. As the disease progresses, memory deficits tend to appear. Reported impairments range from short-term memory deficits to long-term memory difficulties, including deficits in episodic (memory of one’s life), procedural (memory of the body of how to perform an activity) and working memory. Cognitive problems tend to worsen over time, ultimately leading to dementia. This pattern of deficits has been called a subcortical dementia syndrome to distinguish it from the typical effects of cortical dementias e.g. Alzheimer‘s disease.

Reported neuropsychiatric manifestations are anxiety, depression, a reduced display of emotions (blunted affect), egocentrism, aggression, and compulsive behavior, the latter of which can cause or worsen addictions, including alcoholism, gambling, and hypersexuality.  Difficulties in recognizing other people’s negative expressions have also been observed. Prevalence of these symptoms is also highly variable between studies, with estimated rates for lifetime prevalence of psychiatric disorders between 33% and 76%.  For many sufferers and their families these symptoms are among the most distressing aspects of the disease, often affecting daily functioning and constituting reason for institutionalisation. Suicidal thoughts and suicide attempts are more common than in the general population.

Mutant Huntingtin is expressed throughout the body and associated with abnormalities in peripheral tissues that are directly caused by such expression outside the brain. These abnormalities include muscle atrophy, cardiac failure, impaired glucose tolerance, weight loss, osteoporosis and testicular atrophy

Reported prevalences of behavioral and psychiatric symptoms in Huntington’s disease :
Irritability 38–73%
Apathy 34–76%
Anxiety 34–61%
Depressed mood 33–69%
Obsessive and compulsive 10–52%
Psychotic 3–11%

Causes:
Huntington’s disease is caused by a single defective gene on chromosome 4. This leads to damage of the nerve cells in areas of the brain including the basal ganglia and cerebral cortex, and to the gradual onset of physical, mental and emotional changes.

The Huntington’s Disease Association estimates between 6,500 and 8,000 people in the UK have the disease.

The tragedy is that by the time symptoms appear, the person has often had a family and may have passed on the gene to their children. Each person whose parent has Huntington’s disease has a 50 per cent chance of inheriting the gene, and everyone who inherits the gene will at some stage develop the disease.

In three per cent of cases, there’s no family history of Huntington’s disease and the genetic fault may be a new mutation.

The disease can’t be prevented from developing if someone has the faulty gene. To inherit the illness, the gene only has to come from one parent, making it autosomal dominant.

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The gene for Huntington’s disease can be detected with a blood test, which is available to those aged over 18, before symptoms begin. This can determine whether someone has the faulty gene and help them in their family planning

Risk Factors:
If one of your parents has Huntington’s disease, you have a 50 percent chance of developing the disease. In rare cases, you may develop Huntington’s disease without having a family history of the condition. Such an occurrence may be the result of a genetic mutation that happened during your father’s sperm development.

Complications:
After the onset of Huntington’s disease, a person’s functional abilities gradually worsen over time. The rate of disease progression and duration varies. The time from disease onset to death is often about 10 to 30 years. Juvenile onset usually results in death in fewer than 15 years.

The clinical depression associated with Huntington’s disease may increase the risk of suicide. Some research suggests that the greater risk of suicide occurs before a diagnosis is made and in middle stages of the disease when a person has begun to lose independence.

Eventually, a person with Huntington’s disease requires help with all activities of daily living and care. Late in the disease, he or she will likely be confined to a bed and unable to speak. However, a person’s understanding of surroundings and interactions remain intact for a long time.

Common causes of death include:

*Pneumonia or other infections
*Injuries related to falls
*Complications related to the inability to swallow

Diagnosis:
Medical diagnosis of the onset of HD can be made following the appearance of physical symptoms specific to the disease. Genetic testing can be used to confirm a physical diagnosis if there is no family history of HD. Even before the onset of symptoms, genetic testing can confirm if an individual or embryo carries an expanded copy of the trinucleotide repeat in the HTT gene that causes the disease. Genetic counseling is available to provide advice and guidance throughout the testing procedure, and on the implications of a confirmed diagnosis. These implications include the impact on an individual’s psychology, career, family planning decisions, relatives and relationships. Despite the availability of pre-symptomatic testing, only 5% of those at risk of inheriting HD choose to do so

Clinical:
A physical examination, sometimes combined with a psychological examination, can determine whether the onset of the disease has begun. Excessive unintentional movements of any part of the body are often the reason for seeking medical consultation. If these are abrupt and have random timing and distribution, they suggest a diagnosis of HD. Cognitive or psychiatric symptoms are rarely the first diagnosed; they are usually only recognized in hindsight or when they develop further. How far the disease has progressed can be measured using the unified Huntington’s disease rating scale which provides an overall rating system based on motor, behavioral, cognitive, and functional assessments. Medical imaging, such as computerized tomography (CT) and magnetic resonance imaging (MRI), only shows visible cerebral atrophy in the advanced stages of the disease. Functional neuroimaging techniques such as fMRI and PET can show changes in brain activity before the onset of physical symptoms.

Grenetic:
Because HD follows an autosomal dominant pattern of inheritance, there is a strong motivation for individuals who are at risk of inheriting it to seek a diagnosis. The genetic test for HD consists of a blood test which counts the numbers of CAG repeats in each of the HTT alleles.[38] A positive result is not considered a diagnosis, since it may be obtained decades before the symptoms begin. However, a negative test means that the individual does not carry the expanded copy of the gene and will not develop HD.

A pre-symptomatic test is a life-changing event and a very personal decision. The main reason given for choosing testing for HD is to aid in career and family decisions. Over 95% of individuals at risk of inheriting HD do not proceed with testing, mostly because there is no treatment. A key issue is the anxiety an individual experiences about not knowing whether they will eventually develop HD, compared to the impact of a positive result.  Irrespective of the result, stress levels have been found to be lower two years after being tested, but the risk of suicide is increased after a positive test result. Individuals found to have not inherited the disorder may experience survivor guilt with regard to family members who are affected. Other factors taken into account when considering testing include the possibility of discrimination and the implications of a positive result, which usually means a parent has an affected gene and that the individual’s siblings will be at risk of inheriting it. Genetic counseling in HD can provide information, advice and support for initial decision-making, and then, if chosen, throughout all stages of the testing process. Counseling and guidelines on the use of genetic testing for HD have become models for other genetic disorders, such as autosomal dominant cerebellar ataxias. Presymptomatic testing for HD has also influenced testing for other illnesses with genetic variants such as polycystic kidney disease, familial Alzheimer’s disease and breast cancer

Embryonic:
Embryos produced using in vitro fertilisation may be genetically tested for HD using preimplantation genetic diagnosis. This technique, where a single cell is extracted from a 4 to 8 cell embryo and then tested for the genetic abnormality, can then be used to ensure embryos with affected HTT genes are not implanted, and therefore any offspring will not inherit the disease. It is also possible to obtain a prenatal diagnosis for an embryo or fetus in the womb.

Differential diagnosis:
About 90% of HD diagnoses based on the typical symptoms and a family history of the disease are confirmed by genetic testing to have the expanded trinucleotide repeat that causes HD. Most of the remaining are called HD-like disorders.  Most of these other disorders are collectively labelled HD-like (HDL). The cause of most HDL diseases is unknown, but those with known causes are due to mutations in the prion protein gene (HDL1), the junctophilin 3 gene (HDL2), a recessively inherited HTT gene (HDL3—only found in one family and poorly understood), and the gene encoding the TATA box-binding protein (HDL4/SCA17). Other autosomal dominant diseases that can be misdiagnosed as HD are dentatorubral-pallidoluysian atrophy and neuroferritinopathy. There are also autosomal recessive disorders that resemble sporadic cases of HD. Main examples are chorea acanthocytosis, pantothenate kinase-associated neurodegeneration and X-linked McLeod syndrome

Treatment:
There’s no cure, but supportive care can ease many symptoms and help a person with Huntington’s disease, and their family, lead as normal a life as possible.

Drugs can relieve symptoms of involuntary movements, depression and mood swings. Speech therapy can help improve speech and swallowing problems. A high-calorie diet can help maintain weight and improve symptoms such as involuntary movement and behavioural problems.

Cognitive changes often result in loss of enthusiasm, initiative and organisational skills, which can make multi-tasking difficult. Constant nursing care is needed in the later stages of the disease and support for carers is important, too.

Secondary illnesses, such as pneumonia, are often the cause of death.

There’s extensive research into possible treatments for Huntington’s disease. One technique is the use of transplants of foetal brain cells, which appear in some cases to repair and rejuvenate the damaged area.

Meanwhile, researchers at the University of Leeds have found that one of the body’s naturally occurring proteins is causing some of the disruption that occurs in the brains of those with Huntington’s, and its effects may be modified by using drugs that are already being used to help cancer patients. But it is likely to be years, if at all, before these developments result in an effective treatment.

Prognosis:
The length of the trinucleotide repeat accounts for 60% of the variation in the age of onset and the rate of progression of symptoms. A longer repeat results in an earlier age of onset and a faster progression of symptoms. For example, individuals with a trinucleotide repeat greater than sixty repeats often develop the disease before twenty years of age, and those with less than forty repeats may not develop noticeable symptoms. The remaining variation is due to environmental factors and other genes that influence the mechanism of the disease.

Life expectancy in HD is generally around 20 years following the onset of visible symptoms.  Most of the complications that are life-threatening result from muscle coordination issues, or to a lesser extent from behavioural changes resulting from the decline in cognitive function. The largest risk is pneumonia, which is the cause of death of one-third of those with HD. As the ability to synchronise movements deteriorates, difficulty clearing the lungs and an increased risk of aspirating food or drink both increase the risk of contracting pneumonia. The second greatest risk is heart disease, which causes almost a quarter of fatalities of those with HD. Suicide is the next greatest cause of fatalities, with 7.3% of those with HD taking their own lives and up to 27% attempting to do so. It is unclear to what extent suicidal thoughts are influenced by psychiatric symptoms, as they may be considered to be a response of an individual to retain a sense of control of their life or to avoid the later stages of the disease.  Other associated risks include choking, physical injury from falls, and malnutrition.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/huntingtons1.shtml
http://en.wikipedia.org/wiki/Huntington’s_disease
http://www.mayoclinic.com/health/huntingtons-disease/DS00401

http://www.healthtree.com/articles/huntingtons-disease/causes/

http://www.bothbrainsandbeauty.com/academic-discussions/huntingtons-disease-991

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Chili Pepper Ingredient Helps With Weight Loss

Capsaicin, the stuff that gives chili peppers their kick, may cause weight loss and fight fat buildup by triggering certain beneficial protein changes in the body, according to a new study on the topic.
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Jong Won Yun and colleagues point out that obesity is a major public health threat worldwide, linked to diabetes, high blood pressure, heart disease, and other health problems. Laboratory studies have hinted that capsaicin may help fight obesity by decreasing calorie intake, shrinking fat tissue, and lowering fat levels in the blood. Nobody, however, knows exactly how capsaicin might trigger such beneficial effects.

In an effort to find out, the scientists fed high-fat diets with or without capsaicin to lab rats used to study obesity. The capsaicin-treated rats lost 8 percent of their body weight and showed changes in levels of at least 20 key proteins found in fat. The altered proteins work to break down fats. “These changes provide valuable new molecular insights into the mechanism of the anti obesity effects of capsaicin,” the scientists say.

Source: Elements4Health. July 21.2010

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Antibody ‘Fixes Internal Bleeds’

Scientists say they have discovered an antibody that could minimise the major internal bleeding seen in traumas like bullet wounds and car crashes.
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The team at Oklahoma Medical Research Foundation (OMRF) has discovered that a protein called histone is responsible for much of the damage.

They say they have found a specific type of antibody that can block the ability of histone to cause damage.

They say it could lead to new ways to treat diseases and serious injuries.

‘Life threatening’
Writing in the journal, Nature Medicine, the OMRF researchers found that when mice had a bad blood stream infection (sepsis), their blood contained high levels of histones.

They checked this in primates and humans and found the same result.

The histone protein normally sits in the nucleus of a cell, packed around the strands of DNA.

It regulates the DNA, causing it to fold and form the characteristic double helix.


Bullet wounds often lead to severe internal bleeding

When the cell is damaged by injury or disease, the histone is released into the blood system where it begins to kill the lining of blood vessels, causing damage, the OMRF researchers said.

This, they believe, results in uncontrolled internal bleeding and fluid build-up in the tissues, which are life threatening.

Dr Charles Esmon, of OMRF who led the research, said: “When we realised that histones were so toxic, we immediately went to work looking for a way to stop their destructive tendencies.”

Mouse antibody
Marc Monestier, a colleague at Temple University in Philadelphia, had already discovered a specific type of antibody known as a monoclonal antibody that could block the histones.

It had been observed that patients with auto-immune diseases make antibodies to the proteins in their cell nuclei but it was not known why.

This antibody came from a mouse with an auto-immune disease.

The OMRF team have tested the antibody in mice with sepsis and it does stop the toxic effects of the histones and they recover, the researchers say.

They now want to test it in primates and eventually humans.

Dr Esmon said histones were similar in all mammals because they were such basic building blocks.

So a mouse antibody should work equally well in a human.

He said: “We think it was an adaptation during evolution.

“Millions of years ago, when people and animals got ill, they did not die of heart attacks or car accidents they died of infectious diseases.

“Their immune systems went into overdrive throwing everything at it and we believe the histones in the cell nucleus, part of the basic building blocks of life, were the last resort.”

Dr Stephen Prescott, president of OMRF, said: “These findings offer some clues as to why people suffering from one traumatic injury often experience a catastrophic ‘cascade’ of secondary traumatic events.

“If we can figure out how to control the initial injury, perhaps that will stop the domino effect that so often follows.”

Source: BBC News: 26th.Oct.’09

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High-Protein Meals Can Help the Overweight Burn Fat

protein, fat, overweight, weight loss, obesity, atkins

Higher-protein meals may help overweight and obese people burn more fat.

A new study found that overweight men and women burned more post-meal fat when they ate a high-protein breakfast and lunch than when they had lower-protein meals. The added protein seemed to modify the fat-burning deficit seen in heavy individuals.

A number of studies have suggested that high-protein diets may help people shed weight more easily.

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