Rambut Jagung Luruhkan Batu Empedu


Selasa, 16 Juni 2009 | 13:12 WIB

KOMPAS.com - Selama ini Anda mungkin mencari solusi alami untuk mengatasi masalah batu empedu. Bisa jadi rambut jagung adalah pilihannya. Pasalnya, sebagai terapi awal, rambut jagung ternyata memiliki potensi besar untuk meluruhkan batu empedu. Beberapa uji laboratorium telah menguatkan dugaan itu.

Rambut jagung dalam kehidupan sehari-hari lebih dilihat sebagai limbah dari industri pangan maupun rumah tangga. Padahal, seperti diungkapkan ahli tanaman obat Dr.Setiawan Dalimartha, sebagian besar masyrakat sudah memanfaatkan air rebusan rambut jagung sebagai obat tradisional untuk peluruh air seni dan penurun tekanan darah.

Penelitian mengenai kandungan rambut jagung sayangnya masih terbatas dan belum banyak dipublikasi. Namun, beberapa penilitan menunjukan ditemukan adanya kandungan flavonoid yang bermanfaat sebagai peluruh batu empedu.

Sebelum Anda mengonsumsi, pastikan memilih rambut jagung yang masih segar. Maksudnya, pilih jagung yang segar dan ambil rambut jagung yang sebagian masih terbungkus pelepah jagung.

"Jadi bukan yang di luar. Karena rambut jagung bagian dalam jauh lebih bersih dan banyak mengandung zat yang bermanfaat," kata Setiawan.

Tertarik untuk mencoba? Cara meramunya mudah kok.

Peluruh batu empedu
Siapkan 30 gram rambut jagung, rebus dengan air secukupnya. Setelah mendidih, saring airnya lalu dinginkan. Saring kembali, dan setelah dingin dapat diminum. Minum ramuan ini sehari sekali.

Pereda panas dalam
Siapkan 30-40 gram rambut jagung dan irisan daun pandan. Rambut jagung dan daun pandan direbus dengan air secukupnya. Setelah dingin, saring lalu diminum.

Peluruh kencing (diuretik)
Siapkan 30-50 gram rambut jagung dan satu rimpang jahe ukuran sedang. Rebus bahan-bahan dengan air secukupnya. Setelah dingin, saring. Boleh ditambah madu.



http://kesehatan.kompas.com/read/xml/2009/06/16/13122799/rambut.jagung.luruhkan.batu.empedu

DUA CANGKIR TEH HIJAU SETIAP HARI HALAU STROKE

CORBISSEHAT: Jika Anda ingin hidup sehat dan terhindar dari stroke, penelitian membuktikan dua cangkir teh hijau per hari merupakan pilihan yang terbaik.

Minum dua cangkir teh hijau per hari, dapat menghindari serangan stroke yang paling banyak terjadi. Demikian diungkap peneliti asal Australia.

Salah seorang peneliti Profesor Colin Bins dari Schol of Public Health, Curtin University di Australia Barat mengatakan, penelitian yang merek alakukan menunjukkan, orang yang minum minimal satu cangkir teh hijau per hari akan menurunkan risiko terkena stroke ischemic seperti dilansir ABC.net.au, baru-baru ini.

Sementara itu orang yang biasa meminum dua cangkir teh hijau setiap hari dapat menekan risiko hingga 60%. "Dapat dikatakan, jika Anda ingin mengonsumsi secangkir minuman, maka teh merupakan pilihan yang lebh sehat," terangnya.

Jika Anda tidak terlalu menyukai rasa teh hijau, maka teh hitam juga dapat diminum untuk mengurangi risiko stroke. Hanya saja manfaatnya tidak sebanyak yang diperoleh dari teh hijau.

"Kami meyakini teh jenis lain efektivitasnya hanya setengah jika dibandingkan dengan teh hijau untuk mengurangi risiko stroke," tutur Binns.

Dia mengatakan, hasil penelitian ini dapat mmbantu mengurangi kasus stroke yang mengakibatkan kematian sekitar 5 juta orang di seluruh dunia setiap tahun.

Selain itu, penelitian terhadap konsumsi teh hijau diantara para pasien stroke ischemic di Cina selatan, provinsi Guangdong. Ishemic stroke yaitu disebabkan oleh gumpalan lemak yang menghalangi darah ke otak. Stroke jenis ini paling banyak terjadi, sekitar 70% dari seluruh kasus stroke.

Penelitian itu dilakukan dengan dukungan berbagai instansi termasuk Curtin Health Innovation Research Institure dan tiga rumah sakit di Cina yang dilakukan tahun 2007-2008. Studi itu melibatkan 400 pasein yang didiagnosa mengalami stroke dan 400 orang sehat.

Binns mengatakan, penelitian yang dilakukan di Selatan Cina itu sangat penting karena pola makan di kawasan tersebut tidak banyak berubah selama 10-20 tahun terakhir. Populasi daerah itu juga homogen dan minum teh adalah kebiasaan tradisional.

Dia menambahkan, selera orang di Australia seringkali berubah. Sehingga sulit untuk melakukan studi yang serupa. Meskipun demikian, para peneliti meyakini teh hikau akan memiliki manfaat yang serupa jika diterapkan pada pola makan barat. (rin)sumber :http://republika.co.id/berita/55998/Dua_Cangkir_Teh_Hijau_Halau_Stroke


NB: SehatHerbal.com menyediakan Ixora Green Tea- Teh hijua berkualias, harga Rp. 65.000/kotak utk 50 kali pakai.

Info pemesanan : budiprakoso98@gmail.com / 081310343598

Click Here For Shocking Photo's

I am pleased to announce that I suck almost as much at kayaking as I do at trail running.
Our trail kicker friend from Alberta, Willy Bill, came to South-Western Ontario to whip LuLu into shape for our upcoming hike in the wilds of the Yukon.
This included a kayaking trip down the Grand River from Cambridge to Paris.
Normally a slow paddle, the recent deluge of rain caused for a pretty fast current. So much so, that the outfitter we rented some of the kayaks & canoe from, sent along a guide.
( I think he was there to recover the equipment rather than the person.)

All went well until Ken & Jeniffer decided that when coming to a bridge column located in the centre of the river, about at the halfway point, the front paddler wanted to go left of the massive stone structure while the rear paddler wanted the right.
Well the river decided neither and they collided the structure and capsized, causing the guide to earn his keep. He did recover the canoe but Jen & Ken were lost.
Kidding about the last part, they swam ashore and others down river captured their gear as it floated by.

This was a fun way to spend a day since upon 'Two Beer Nancy's' demand, we then proceeded to a licensed establishment to sample some beverages and chicken wings.

The evening concluded with a BBQ back in London to solve the worlds problems.

On a Trail Running note, our motley crew took home the hardware at Sulphur Springs Trail Races.
And I can't wait till Alita comes out to Saturday morning trail runs wearing her Sulphur Springs shirt.
Coming up in the OUS is Niagara Ultra on June 20th.
https://www.onlineregistrations.ca/niagara/
Sorry no trails here, but a fast course for a 10k,25k, marathon and 50K
Great prizes that come from local wineries and early entries get a warm hoodie.
And rumour has it that there may be some beer to be had at the end.
And speaking of beer.. Creemore Vertical Challenge is on July 4th. If you like scenery and hills..never ending freaking hills.. then this is the race to do.
The only thing that compels me to do this race is that the kegs of Creemore are at the finish line.
http://www.onlineregistrations.ca/creemore/

The Coronary Heart Disease Epidemic: Possible Culprits Part I

In the last post, I reviewed two studies that suggested heart attacks were rare in the U.K. until the 1920s -1930s. In this post, I'll be discussing some of the diet and lifestyle factors that preceded and associated with the coronary heart disease epidemic in the U.K and U.S. I've cherry picked factors that I believe could have played a causal role. Many things changed during that time period, and I don't want to give the impression that I have "the answer". I'm simply presenting ideas for thought and discussion.

First on the list: sugar. Here's a graph of refined sugar consumption in the U.K. from 1815 to 1955, from the book The Saccharine Disease, by Dr. T. L. Cleave. Sugar consumption increased dramatically in the U.K. over this time period, reaching near-modern levels by the turn of the century, and continuing to increase after that except during the wars: Here's a graph of total sweetener consumption in the U.S. from 1909 to 2005 (source: USDA food supply database). Between 1909 and 1922, sweetener consumption increased by 40%:

If we assume a 10 to 20 year lag period, sugar is well placed to play a role in the CHD epidemic. Sugar is easy to pick on. Diets high in refined sugar tend to promote obesity due to overeating.  An excess causes a number of detrimental changes in animal models and human subjects that are partially dependent on the development of obesity, including fatty liver, the metabolic syndrome, and small, oxidized low-density lipoprotein particles (LDL). Small and oxidized LDL associate strongly with cardiovascular disease risk and may be involved in causing it. These effects seem to be partly attributable to the fructose portion of sugar, which is 50% of table sugar (sucrose), about 50% of most naturally sweet foods, and 55% of the most common form of high-fructose corn syrup. That explains why starches, which break down into glucose (another type of sugar), don't have the same negative effects as table sugar and HFCS.

Hydrogenated fat is the next suspect. I don't have any graphs to present, because no one has systematically tracked hydrogenated fat consumption in the U.S. or U.K. to my knowledge. However, it was first marketed in the U.S. by Procter & Gamble under the brand name Crisco in 1911. Crisco stands for "crystallized cottonseed oil", and involves taking an industrial waste oil (from cotton seeds) and chemically treating it using high temperature, a nickel catalyst and hydrogen gas (see this post for more information). Hydrogenated fats for human consumption hit markets in the U.K. around 1920. Here's what Dr. Robert Finlayson had to say about margarine in his paper "Ischaemic Heart Disease, Aortic Aneurysms, and Atherosclerosis in the City of London, 1868-1982":

...between 1909-13 and 1924-28, margarine consumption showed the highest percentage increase, whilst that of eggs only increased slightly and that of butter remained unchanged. Between 1928 and 1934, margarine consumption fell by one-third, while butter consumption increased by 57 percent: and increase that coincided with a fall of 48 percent in its price. Subsequently, margarine sales have burgeoned, and if one is correct in stating that the coronary heart disease epidemic started in the second decade of this century, then the concept of hydrogenated margarines as an important aetiological factor, so strongly advocated by Martin, may merit more consideration than hitherto.

Partially hydrogenated oils contain trans fat, which is truly new to the human diet, with the exception of small amounts found in ruminant fats including butter. But for the most part, natural trans fats are not the same as industrial trans fats, and in fact some of them, such as conjugated linoleic acid (CLA), may be beneficial. To my knowledge, no one has discovered health benefits of industrial trans fats. To the contrary, compared to butter, they shrink LDL size. They also inhibit enzymes that the body uses to make a diverse class of signaling compounds known as eicosanoids. Trans fat consumption associates very strongly with the risk of heart attack in observational studies. Which is ironic, because hydrogenated fats were originally marketed as a healthier alternative to animal fats. The Center for Science in the Public Interest shamed McDonald's into switching the beef tallow in their deep friers for hydrogenated vegetable fats in the 1990s. In 2009, even the staunchest opponents of animal fats have to admit that they're healthier than hydrogenated fat.
The rise of cigarettes was a major change that probably contributed massively to the CHD epidemic. They were introduced just after the turn of the century in the U.S. and U.K., and rapidly became fashionable (source):
If you look at the second to last graph from the previous post, you can see that there's a striking correspondence between cigarette consumption and CHD deaths in the U.K. In fact, if you moved the line representing cigarette consumption to the right by about 20 years, it would overlap almost perfectly with CHD deaths. The risk of heart attack is so strongly associated with smoking in observational studies that even I believe it probably represents a causal relationship. There's no doubt in my mind that smoking cigarettes contributes to the risk of heart attack and various other health problems.

Smoking is a powerful factor, but it doesn't explain everything. How is it that the Kitavans of Papua New Guinea, more than 3/4 of whom smoke cigarettes, have an undetectable incidence of heart attack and stroke? Why do the French and the Japanese, who smoke like chimneys (at least until recently), have the two lowest heart attack death rates of all the affluent nations? There's clearly another factor involved that trumps cigarette smoke. 

The Coronary Heart Disease Epidemic

Few people alive today are old enough to remember the beginning of the coronary heart disease (CHD) epidemic in the 1920s and 1930s, when physicians in the U.S. and U.K. began sounding alarm bells that an uncommon disease was rapidly becoming the leading cause of death. By the 1950s, their predictions had come true. A decade later, a new generation of physicians replaced their predecessors and began to doubt that heart attacks had ever been uncommon. Gradually, the idea that the disease was once uncommon faded from the public consciousness, and heart attacks were seen as an eternal plague of humankind, avoided only by dying of something else first.

According to U.S. National Vital Statistics records beginning in 1900, CHD was rarely given as the cause of death by physicians until after 1930. The following graph is from The Great Cholesterol Con, by Anthony Colpo.


The relevant line for CHD deaths begins in the lower left-hand part of the graph. Other types of heart disease, such as heart failure due to cardiomyopathy, were fairly common and well recognized at the time. These data are highly susceptible to bias because they depend on the physician's perception of the cause of death, and are not adjusted for the mean age of the population. In other words, if a diagnosis of CHD wasn't "popular" in 1920, its prevalence could have been underestimated. The invention of new technologies such as the electrocardiogram facilitated diagnosis. Changes in diagnostic criteria also affected the data; you can see them as discontinuities in 1948, 1968 and 1979. For these reasons, the trend above isn't a serious challenge to the idea that CHD has always been a common cause of death in humans who reach a certain age.

This idea was weakened in 1951 with the publication of a paper in the Lancet medical journal titled "Recent History of Coronary Disease", by Dr. Jerry N. Morris. Dr. Morris sifted through the autopsy records of London Hospital and recorded the frequency of coronary thrombosis (artery blockage in the heart) and myocardial infarction (MI; loss of oxygen to the heart muscle) over the period 1907-1949. MI is the technical term for a heart attack, and it can be caused by coronary thrombosis. Europe has a long history of autopsy study, and London Hospital had a long-standing policy of routine autopsies during which they kept detailed records of the state of the heart and coronary arteries. Here's what he found:

The dashed line is the relevant one. This is a massive increase in the prevalence of CHD death that cannot be explained by changes in average lifespan. Although the average lifespan increased considerably over that time period, most of the increase was due to reduced infant mortality. The graph only includes autopsies performed on people 35-70 years old. Life expectancy at age 35 changed by less than 10 years over the same time period. The other possible source of bias is in the diagnosis. Physicians may have been less likely to search for signs of MI when the diagnosis was not "popular". Morris addresses this in the paper:

The first possibility, of course, is that the increase is not real but merely reflects better post-mortem diagnosis. This is an unlikely explanation. There is abundant evidence throughout the forty years that the department was fully aware of the relation of infarction to thrombosis, of myocardial fibrosis to gradual occlusion, and of the topical pathology of ostial stenosis and infarction from embolism, as indeed were many pathologists last century... But what makes figures like these important is that, unlike other series of this kind, they are based on the routine examination at necropsy of the myocardium and of the coronary arteries over the whole period. Moreover Prof. H. M. Turnbull, director of the department, was making a special case of atheroma and arterial disease in general during 1907-1914 (Turnbull 1915). The possibility that cases were overlooked is therefore small, and the earlier material is as likely to be reliable as the later.

Dr. Morris's study was followed by another similar one published in 1985 in the journal Medical History, titled "Ischaemic Heart Disease, Aortic Aneurysms, and Atherosclerosis in the City of London, 1868-1982", conducted by Dr. Robert Finlayson. This study, in my opinion, is the coup de grace. Finlayson systematically scrutinized autopsy reports from St. Bartholemew's hospital, which had conducted routine and detailed cardiac autopsies since 1868, and applied modern diagnostic criteria to the records. He also compared the records from St. Bartholemew's to those from the city mortuary. Here's what he found:

The solid line is MI mortality. Striking, isn't it? The other lines are tobacco and cigarette consumption. These data are not age-adjusted, but if you look at the raw data tables provided in the paper, some of which are grouped by age, it's clear that average lifespan doesn't explain much of the change. Heart attacks are largely an occurrence of the last 80 years.

What caused the epidemic? Both Drs. Morris and Finlayson also collected data on the prevalence of atherosclerosis (plaques in the arteries) over the same time period. Dr. Morris concluded that the prevalence of severe atherosclerosis had decreased by about 50% (although mild atherosclerosis such as fatty streaks had increased), while Dr. Finlayson found that it had remained approximately the same:


He found the same trend in females. This casts doubt on the idea that coronary atherosclerosis is sufficient in and of itself to cause heart attacks, although modern studies have found a strong association between advanced atherosclerosis and the risk of heart attack on an individual level. Heart attacks are caused by several factors, one of which is atherosclerosis.  

What changes in diet and lifestyle associated with the explosion of MI in the U.K. and U.S. after 1920? Dr. Finlayson has given us a hint in the graph above: cigarette consumption increased dramatically over the same time period, and closely paralleled MI mortality. Smoking cigarettes is very strongly associated with heart attacks in observational studies. Animal studies also support the theory. While I believe cigarettes are an important factor, I do not believe they are the only cause of the MI epidemic. Dr. Finlayson touched on a few other factors in the text of the paper, and of course I have my own two cents to add. I'll discuss that next time.