On celery, seduction, science and salad

Recently, I posted a little poem by Ogden Nash on my Facebook page.

celery by ogden nash www.cookingforhealth.biz

Seeing this, one of my friends asked me about the health benefits of celery and whether it makes any difference if you eat it raw or cooked.

So here are some answers to these questions.

But first some celery background and a story of seduction.

Botany and history

Celery (Apium graveolens L.) is a member of the same botanical family as carrots, parsley and fennel – the Umbelliferae.

celery botanical drawing

Celery is a member of the Umbelliferae

Modern celery originated from wild celery, native to the Mediterranean, where its seeds were once widely used as a medicine (1).  It was not cultivated as a food plant until 1623.

Wild celery was mentioned in Homer’s Odyssey in about 850 BCE (2).

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Odysseus and his companions were on their way to their beloved Ithaca, but Poseidon, the moody god of the seas, became angry with the hero. So he sank all the ships of Odysseus and drowned his companions.

Shipwrecked, Odysseus was tortured for nine days and nights, until the waves took him to a beautiful island called Ogygia, believed to be in Western Europe.

There he was seduced by a nymph called Calypso, who fell in love with him and would not allow him to leave.

Jan Brueghel-Calypso's Cave

Calypso’s Cave by Jan Brueghel

Eventually, after seven years, Zeus – King of the gods – sent his messenger Hermes to tell Calypso to let Odysseus go.

So Hermes travelled over the endless breakers, until he reached the distant isle, then leaving the violet sea he crossed the land, and came to the vast cave where the nymph of the lovely tresses lived, and found her at home.

A great fire blazed on the hearth, and the scent of burning cedar logs and juniper spread far across the isle. Sweet-voiced Calypso was singing within, moving to and fro at her loom, weaving with a golden shuttle. Around the cave grew a thick copse of alder, poplar and fragrant cypress, where large birds nested, owls, and falcons, and long-necked cormorants whose business is with the sea. And heavy with clustered grapes a mature cultivated vine went trailing across the hollow entrance. And four neighbouring springs, channelled this way and that, flowed with crystal water, and all around in soft meadows iris and wild celery flourished.

Celery was considered an aphrodisiac by the Ancient Greeks and Romans (3).

Some have speculated that Calypso was rendered ravenous by her celery-rich diet and pounced on Odysseus, detaining him for years of amorous activity.

Is there any scientific evidence to support the use of celery as an aphrodisiac?

More on that later.

There is however no doubt that, for whatever reason, celery was highly prized in ancient times and its leaves were used as garlands for the winners at the Isthmian and Nemean games.

In both Ancient Greece and Ancient Egypt, celery leaves were also used as garlands for the dead. Dried inflorescences and leaves of celery were reportedly found in the tomb of Tutankhamun (4).

But back to the story…

Calypso was not best pleased when Hermes explained his mission. She ranted and raved and accused him of jealousy.

Realising, however, that it was futile to argue with Zeus, Calypso sorrowfully followed the order.

She gave Odysseus enough tools to build a solid raft.

Odysseus loaded the raft with plenty of water and food and finally made his farewells to embark on a world of new adventures.

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Health benefits of celery

So what can celery do for you?

My friend said he thought celery was a pointless food – nothing but water, which takes more energy to digest than it provides.

How true is this perception?

Nutritional content of celery

Well it is true that celery contains a lot of water – 95 per cent water to be precise.

Celery is also, however, rich in vitamin C and fibre. It is a very good source of potassium, folic acid and vitamins B6 and B1; and a good source of calcium and vitamin B2 (5).

Whilst celery does contain more sodium than other vegetables, this is offset by very high levels of potassium.

One 8-inch (20 cm) celery stalk contains approximately 32 milligrams of sodium and 104 milligrams of potassium, whilst providing only 6 calories as carbohydrate (5).

This reminds me to address one common question about celery.

Celery stalks www.cookingforhealth.biz

Is it true that you burn more calories eating celery than it provides?

A search of the internet uncovers all manner of speculation on this subject but very little scientific evidence to support it.

What we do know from science is that approximately 10 per cent of the calories we consume each day are used up in the process of eating and digesting food.

This energy ‘waste’ is called the thermogenic effect of food, dietary-induced thermogenesis, the ‘specific heat of feeding’, or the thermic effect of food.

All this means is that every time we eat, some of the calories contained in the food are lost as heat.

The exact amount of heat lost during eating can be measured by putting someone in a whole body calorimeter, giving them food to eat, and recording the change in temperature.

To my knowledge, nobody has actually measured a person’s heat production after eating a meal of celery alone, so we are left to guess what might happen from the results of other experiments.

Measurements show that some foods are digested with little heat loss, for example, fat-based foods.

High protein foods are the opposite and generate a lot of heat – presumably because the body has to work harder to digest protein.

Celery consists of mostly water and fibre. So what is the thermogenic effect of water and fibre?

Almost nothing.

In fact, if you put someone in a whole body calorimeter and give them a high-fibre diet, their post-food heat production is actually reduced compared to a normal diet (6)(7)(8).

Supplementing a balanced 240 kcal meal with 3 grams of fibre (equivalent of five celery stalks) reduces the overall thermogenic effect of the meal by 19 kcal. This effectively means that of the 30 calories gained from eating your celery stalks, 19 calories fewer are used processing it than if it did not have the fibre in it.

So, after being chewed, the fibre in celery gets passed through the gut and out the other end without the body doing too much to it on the way. Although it may take you a while to chew the celery stalks, the gut does not waste much time on it.

So, sorry dieters, but it is unlikely that eating celery burns more calories than it provides.

You could go for a walk whilst munching celery; that would work.

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For those of you who like geeky information, here is a detailed breakdown of the nutrients in raw celery.

Nutrient Unit   Value per 100 g
     
Water g 95.43
Energy kcal 16
Protein g 0.69
Total lipid (fat) g 0.17
Carbohydrate, by difference g 2.97
Fibre, total dietary g 1.6
Sugars, total g 1.83
     
Minerals    
Calcium, Ca mg 40
Iron, Fe mg 0.2
Magnesium, Mg mg 11
Phosphorus, P mg 24
Potassium, K mg 260
Sodium, Na mg 80
Zinc, Zn mg 0.13
     
Vitamins    
Vitamin C, total ascorbic acid mg 3.1
Thiamin mg 0.021
Riboflavin mg 0.057
Niacin mg 0.32
Vitamin B-6 mg 0.074
Folate, DFE µg 36
Vitamin B-12 µg 0
Vitamin A, RAE µg 22
Vitamin A, IU IU 449
Vitamin E (alpha-tocopherol) mg 0.27
Vitamin D (D2 + D3) µg 0
Vitamin D IU 0
Vitamin K (phylloquinone) µg 29.3
     
Lipids    
Fatty acids, total saturated g 0.042
Fatty acids, total monounsaturated g 0.032
Fatty acids, total polyunsaturated g 0.079
Cholesterol mg 0
     

Phytochemical content

In addition to the nutrients listed above, celery contains literally hundreds of powerful phytochemicals (9).

Celery seeds contain 1.5 to 3 per cent volatile oil responsible for the characteristic aroma of celery.  The chemical constituent of celery seed volatile oil was found to be 60–70 per cent limonene, phthalides and β-salinene, coumarins, furanocoumarins (bergapten) and flavonoids (apiin, apigenin).

Some of the phytochemicals identified in celery are listed below (10).

Compound
Percentage
Limonene
72.16
beta-Selinene
12.17
n-butyl phthalide
2.56
Lingustilide
2.41
alpha-Selinene
2.05
Linalool
1.48
alpha-Pinene
1.05
Myrcene
0.95
Sabenene
0.76
r-Cymene
0.74
Epoxycaryophyllene
0.55
Eudesmol
0.29
Caryophyllene
0.17
Thymol
0.17
Isopulegone
0.16
Cinnamic aldehyde
0.15
Carvone
0.09
alpha-lonone
0.05
Geranyl acetate
0.04
beta-Phellandrene
0.02
Pentyl benzene
0.02
Camphene
Traces
beta-Pinene
Traces
3-carene
Traces
alpha-Phellandrene
Traces
(Cis) beta-Ocimene
Traces
(Trans)beta-Ocimene
Traces

Use as a herbal medicine

Traditionally, wild celery was used as an herbal medicine with a range of alleged properties (11) (12), including:

  • Aphrodisiac
  • Anthelmintic
  • Anti-inflammatory, for rheumatic conditions
  • Antiseptic, especially for urinary tract infections
  • Antispasmodic,
  • Carminative – prevents formation of gas in the gastrointestinal tract or facilitates the expulsion of said gas, thereby combating flatulence
  • Diuretic
  • Emmenagogue, stimulates blood flow in the pelvic area and uterus
  • Laxative
  • Sedative
  • Stimulant
  • Tonic

Modern scientific studies have revealed that many of the phytochemicals found in celery and other plants possess interesting biological activity (13).

It is important to note that most studies to date have used animal models and effects in humans have yet to be proven.

That said, there is some interesting evidence developing for various potential health benefits of celery.

Celery seed

Celery seed

Scientific evidence for health benefits of celery

Anti-hypertensive – lowers blood pressure

In animal studies, extracts of celery have been shown to reduce blood pressure (14, 15).

The flavone apigenin and the isobenzofuranone, 3-n-butylphthalide, are two of the phytochemicals best studied in this respect.

In one experiment, a very small amount of 3-n-butylphthalide, equivalent to that in four stalks of celery, lowered blood pressure by 12 to 14 per cent (16).

In animals, 3-n-butylphthalide appears to lower blood pressure by acting as both a diuretic and vasodilator (causes the blood vessels to expand) by influencing the production of hormone-like substances called prostaglandins, as well as acting in a similar manner to calcium-channel blockers (17).

Apigenin has also been shown to affect vasodilation by stimulating calcium channels in rat cell membranes (18).

Hypolipidemic – lowers cholesterol and triglycerides

3-n-butylphthalate has also been shown to lower blood cholesterol levels and reduce the formation of arterial plaque in preclinical studies (animal and in vitro studies) (19) (20).

This effect may increase the elasticity of blood vessels and also lead to lower blood pressure readings.

3-n-butylphthalate also appears to promote some effects on areas and systems of the brain that control vascular resistance (21).

Other studies in rats show that extracts of celery, containing terpenoid, tannin, alkaloid, glycoside, flavonoid and sterol phytochemicals, dose dependently inhibited total cholesterol, triglycerides, and low density lipoprotein levels, and significantly increased high density lipoprotein level (22).

Celery leaves

Celery leaves

Anti-inflammatory – reduces inflammation

Extracts of celery have been investigated and found to have significant anti-inflammatory activity in animal models (23) (24).

It is proposed that the anti-inflammatory activity of celery may form a basis for the reputation of the plant as a medicinal treatment for rheumatic and arthritic diseases.

Flavonoids are reported to affect the inflammatory process and to possess anti-inflammatory as well as immunomodulatory activity in vitro and in vivo.

Since nitric oxide produced by inducible nitric oxide synthase is one of the inflammatory mediators, the effects of celery extracts containing the flavonoid apiin as a major constituent, on inducible nitric oxide synthase expression and nitric oxide production were evaluated in a cell line (25).

The extract, and apiin alone, showed significant inhibitory activity on nitrite (NO) production.

Further tests on mice showed that the extract exerted anti-inflammatory activity in vivo, with a potency seven-times lower than that of indometacin, the non-steroidal anti-inflammatory drug used as reference (25).

Luteolin, another flavonoid found in celery, demonstrates a spectrum of biological activities.

Some Chinese researchers looked at the anti-inflammatory activity of luteolin in acute and chronic models in mice.  They observed suppression of inflammation in vivo (26).

Further experiments provided evidence that luteolin  may be a potent selective inhibitor of cyclooxygenase-2 (COX-2), which is the same target as that of the non-steroidal anti-inflammatory drugs (26).

celery-flowers

Celery flowers

Anti-cancer

Many of the phytochemicals in celery are the subject of research for their potential anti-cancer activities (27)(28).

Luteolin, for example, is a flavonoid found in celery. It has been found to inhibit angiogenesis, induce apoptosis, prevent carcinogenesis in animal models, reduce tumour growth in vivo and to sensitize tumour cells to the cytotoxic effects of some anticancer drugs (29)(30).

Apigenin in celery has also been shown to regulate the cell cycle and thus may have benefits for cancer prevention (31).

Extracts of celery have been found to protect against chemically induced liver cancer in animal models (32).

Di(2-ethylhexyl) phthalate (DEHP), the most abundant phthalate in the environment, is known to be a reproductive toxicant. Researchers in Egypt investigated whether celery oil affects DEHP-induced testicular toxicity.  They found that celery oil partially prevented the damaging effects of this environmental toxin (33).

Antiulcerogenic – inhibits stomach ulcers

Celery oil was found to inhibit stomach ulcers in a dose-dependent manner in experimental rats, which was similar to that induced by omeprazole, a widely used drug for indigestion, acid reflux and peptic ulcers (34).  The major phyochemicals identified were β-pinene, camphene, cumene, limonene, α-thuyene, α-pinene, β-phellendrene, p-cymene, γ-terpinene, sabinene and terpinolene.

In another study with rats, pretreatment with celery extract produced dose-dependent reduction in all experimentally induced gastric lesions, with no toxic side effects or mortality over a period of 14 days. The phytochemical screening showed the presence of flavonoids, tannins, volatile oils, alkaloids, sterols and/or triterpenes. The authors concluded that celery extract significantly protects the gastric mucosa and suppresses the basal gastric secretion in rats, possibly through its antioxidant potential (35).

Celery stalks

Celery stalks

Anti-oxidant activity

Dietary plants contain variable chemical families and amounts of antioxidants.  Celery is no exception.

Antioxidants can eliminate free radicals and other reactive oxygen and nitrogen species, and these reactive species contribute to most chronic diseases. It is hypothesized that antioxidants originating from foods may work as antioxidants in their own right in vivo, as well as bring about beneficial health effects through other mechanisms, including acting as inducers of mechanisms related to antioxidant defence, longevity, cell maintenance and DNA repair (36).

The antioxidant content of celery products compared with broccoli and blueberries is shown below (36).

It is important to note the considerable variability between samples depending on environment, cultivar and type of product.

Product Antioxidant content
  mmol per 100g
Celery seeds 8.17
Celery leaves, dried 16.91
Celery raw, USA 0.06
Celery raw, Mali 0.81
Celery blanched 0
Broccoli raw, Norway 0.85
Broccoli raw, USA 0.25
Broccoli raw, Spain 0.68
Blueberries, cultivated USA 1.85
Blueberries, cultivated Norway 1.26

Anti-microbial activity

Celery is reported to have anti-bacterial and weak anti-fungal activity.

Celery extracts have been shown to have potent activity against Helicobacter pylori, a gram-negative bacterium found in the stomach (37).  H. pylori has been associated with chronic gastritis and gastric ulcers, conditions that were not previously believed to have a microbial cause. It is also linked to the development of duodenal ulcers and stomach cancer, though 80 per cent of people infected display no disease symptoms.

Essential oil of celery has also been shown to be strongly inhibitory against Escherichia coli and moderately inhibitory against Pseudomonas aeruginosa and Staphylococcus aureus (34).

Moderate anti-microbial activity has been shown by extracts of celery against multi-drug resistant Salmonella typhi (38).

This anti-microbial activity may explain the use of celery as a traditional herbal remedy for urinary tract and other infections.

Alzheimer’s disease

Alzheimer’s disease is an age-related, progressive neurodegenerative disorder that occurs gradually and results in memory, behaviour, and personality changes.

L-3-n-butylphthalide, an extract from seeds of celery, has been shown to have neuroprotective effects on ischaemic, vascular dementia, and amyloid-beta-infused animal models (39).

Treatment with L-3-n-butylphthalide significantly improved the spatial learning and memory deficits of transgenic mice compared to the controls.

It is believed to do this by inhibiting oxidative injury, neuronal apoptosis and glial activation, regulating amyloid-β protein precursor (AβPP) processing and reducing Aβ generation (40).

Celery root

Celery root

Multiple sclerosis

Multiple sclerosis is an inflammatory and demyelinating disease of the central nervous system which mainly affects young adults.

An animal model of multiple sclerosis called experimental allergic encephalomyelitis is used to test potential treatments for this disease.

In Iran, a herbal-marine product called MS14, containing 90 per cent Penaeus latisculatus (Western King prawn), 5 per cent Apium graveolens (celery), and 5 per cent Hypericum perforatum L (St John’s Wort) is used to slow down or halt the progression of multiple sclerosis.

Mice with induced brain inflammation were fed a diet containing MS14 (30 per cent) and monitored for 20 days. The disease was slowed down in the treated mice relative to the controls.  Moreover, while there were moderate to severe neuropathological changes in the controls, milder changes were seen in the mice treated with MS14 (41).

The precise role of celery in this remedy has not been elucidated and a great deal more work is required to determine its value for this indication.

Aphrodisiac

Earlier I recounted the story of Calypso and Odysseus, full of desire in their celery-adorned cave.

This is not the only myth implicating celery as an aphrodisiac (42).

Central to the Celtic legend of Tristan and Isolde is a love potion, which they accidentally consume and are overcome with passion. This is unfortunate as Tristan is escorting Isolde on her way to marry his uncle.

Some say that their magic philtre contained celery root, though there is no direct evidence for this.  Love potions were usually made from mandrake (love apples), a poisonous member of the nightshade family, with other ingredients including orange, ambergris, vervain, briony and fern seed.

Tristan and Isolde drinking the love potion by John William Waterhouse

Tristan and Isolde drinking the love potion by John William Waterhouse

In the 18th century, Grimod de la Reyniere, an early food journalist, warned of celery’s aphrodisiac properties, advising that

it is not in any way a salad for bachelors

It is rumoured that Madame de Pompadour, maverick mistress of King Louis XV, invented a celery soup to inflame the desires of her royal lover.

So is there any scientific evidence to support these claims?

In 1979, two researchers reported that they had identified the volatile steroid, 5 alpha-androst-16-en-3-one, in the cytoplasm of parsnip and celery at concentrations of 8 nanograms per gram (8 parts per billion) (43).

This steroid is a pheromone found in both human male and female sweat and urine.  It is also found in high concentrations in the saliva of male pigs, and, when sniffed by a female pig that is in heat, results in the female assuming the mating stance.  Androstenone is the active ingredient in ‘Boarmate’, a commercial product made by DuPont sold to pig farmers to test sows for timing of artificial insemination.

mating pigs

Androstenone was the first mammalian pheromone to be identified and has thus been the subject of considerable study.

It turns out that the ability to smell androstenone is genetically determined (44).

Some people cannot smell it at all, whilst others can detect it down to levels of 0.2 parts per billion, which is 40 times lower than the concentration of androstenone reported in celery.

The speculation is that the smell of androstenone in celery acts as an aphrodisiac in sensitive individuals, though there is no direct evidence to confirm this.

The other speculation is that the action of certain phytochemicals in celery as potent vasodilators, as described above in the section on blood pressure (17), enhances male erectile function and thus sexual potency.

Again, however, there is no direct evidence to substantiate this hypothesis and, on the whole, scientists are dismissive of claims of the aphrodisiac properties of plants (45).

This does not necessarily mean that scientists are right – this is a notoriously difficult subject to study and research funding for it is hard to obtain – so, until more data are available, you will have to conduct your own experiments…

Adverse effects of celery

Celery produces phytochemicals called psoralens, which are furanocoumarins (46).

Psoralens are believed to be phytoalexins associated with celery resistance to pathogens.  High levels of psoralens are produced by celery infected with fungal pathogens.

When these compounds are exposed to long-wave UV light or sunlight the phototoxic furanocoumarins become carcinogenic agents; recognized as causally-related to skin cancer by the World Health Organization.

Photodermatitis of the fingers, hands and forearms is therefore a known occupational risk for celery handlers and field workers (47).

celery field workers

Workers in grocery stores and agricultural workers have also been reported to suffer skin reactions after handling celery and being exposed to UV light.

One case reported in the medical literature involved a 65-year-old woman who developed a severe, generalized phototoxic reaction following a visit to a suntan parlour. History taking revealed that she had consumed a large quantity of celery root one hour earlier.

Some people suffer allergic reactions to celery, caused by a protein called Api g 2; exposure can produce mild symptoms of skin irritation or cause potentially fatal anaphylactic shock.

Cooking celery does not destroy the proteins which cause the allergic reaction.

Allergy to celery seems to be linked to people with seasonal hay fever to birch and/or mugwort pollen (usually March/April) (47). This is called cross-reaction and is often an important cause of food allergies.

Celery allergy seems to be far more common in central Europe, mainly France, Switzerland and Germany, and less so in the UK and US, where peanut allergy is the most common.

Should you eat celery raw or cooked?

From a purely nutritional point of view, it is generally the case that storage and cooking of vegetables leads to loss of nutrients. The bioavailability of some nutrients, such as iron, may however be increased by cooking (48).

Loss of vitamins and minerals from vegetables is mainly because of extraction into the cooking liquid rather than their destruction. So provided that you consume the cooking liquid, as you do with soups and casseroles for example, you will still benefit from the nutrients.

Phytochemicals vary substantially in their stability to temperature, light and pH (49).

In general, the less food plants are processed and cooked the more phytochemicals remain active, but this is not always the case.

Spanish scientists investigated the influence of home cooking methods (boiling, microwaving, pressure-cooking, griddling, frying, and baking) on antioxidant activity in 20 vegetables (50).

Artichoke was the only vegetable that kept its very high antioxidant activity in all the cooking methods.

Highest losses of antioxidant activity were observed in cauliflower after boiling and microwaving; pea after boiling; courgette (zucchini) after boiling and frying; and swiss chard and pepper with all methods.

Beetroot, green bean, and garlic kept their antioxidant activity after most cooking treatments.

Celery reportedly increased its antioxidant capacity in all the cooking methods, except boiling when it lost 14 per cent.

Whether to eat celery raw or cooked is a matter of personal choice and depends on your preferences, your constitution, your condition at the time and your external environment.

In hot weather, raw celery is very cooling.

When the weather is cooler or if your digestive system is weak, it may be better to eat cooked celery in a soup or casserole.

Recipes with celery

Raw celery can be used in salads, as crudites to eat with vegetable dips, and as an ingredient in a refreshing green juice.

Cooked celery can be used in soups, sauces and casseroles.

Celery, cucumber, apple, parsley and lime juice

Green juices are a great way to include a wider variety of vegetables in your diet, are packed with nutrients and easy to digest.

Here is a delicious recipe for a refreshing, cooling green juice, ideal for a hot day.

Please click here for details: Recipe for celery, cucumber, apple, parsley and lime juice.

celery cucumber apple lime parsley juice www.cookingforhealth.biz

Celery, cucumber, apple, parsley and lime juice – Jane Philpott at http://www.cookingforhealth.biz

Pressed salad with celery, cucumber, fennel and radish

On the hottest days, we need to balance the external heat by using raw vegetables with cooling properties.  This crunchy, tangy salad using celery is easy to prepare and ideal for al fresco meals.

Please click here for details: Recipe for celery, fennel, cucumber and radish pressed salad

close up celery fennel cucumber radish salad www.cookingforhealth.biz

Celery and sweetcorn chowder

This simple, sweet, summery soup recipe can be served warm or cold.  It soothes the digestive system and helps to relax you at the start of a meal.

Please click here for details: Recipe for celery and sweetcorn chowder.

celery and sweetcorn chowder www.cookingforhealth.biz

Celery and sweetcorn chowder – Jane Philpott at http://www.cookingforhealth.biz

And finally…

Given that I have just devoted a whole blog post to extolling the virtues of celery, do I think you should rush off and start buying wholesale quantities?

Of course not.

That would be silly.

Why?

The reason is that I could choose almost any food plant and write a similar article about all the wonderful nutrients and phytochemicals it contains and the beneficial effects of these substances on your health.

All plants contain an incredible array of substances with powerful biological activity, which protect our bodies from damage and help to prevent and treat chronic disease.

These substances vary from plant to plant and it is the COMBINATION of all of them, operating together in a coordinated and often synergistic manner to regulate gene expression, which results in optimum health.

So just make sure you eat as many whole plant foods as possible and you will maximise your chances of living a long and healthy life.

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References

(1)  Rubatzky, V.E. and Yamaguchi, M. (1997), World Vegetables, second edition, N.Y. Chapman & Hall, pp. 432–443.

(2) Homer, the Odyssey, Book V, 71-82

(3) Domeena C. Renshaw. Aphrodisiacs: The Science and the Myth. JAMA. 1986;255(1):98-99. doi:10.1001/jama.1986.03370010108037

(4) D. Zohary and M. Hopf, Domestication of Plants in the Old World, (3rd ed. 2000) p.202.

(5) U.S. Department of Agriculture, Agricultural Research Service. 2012. USDA National Nutrient Database for Standard Reference, Release 25. Nutrient Data Laboratory Home Page, http://www.ars.usda.gov/nutrientdata

(6) Mikkelsen PB, Toubro S, & Astrup A (2000). Effect of fat-reduced diets on 24-h energy expenditure: comparisons between animal protein, vegetable protein, and carbohydrate. The American journal of clinical nutrition, 72 (5), 1135-41 PMID: 11063440

(7) Raben A, Christensen NJ, Madsen J, Holst JJ, & Astrup A (1994). Decreased postprandial thermogenesis and fat oxidation but increased fullness after a high-fiber meal compared with a low-fiber meal. The American journal of clinical nutrition, 59 (6), 1386-94 PMID: 8198065

(8) Westerterp, K. (2004). Diet induced thermogenesis Nutrition & Metabolism, 1 (1) DOI: 10.1186/1743-7075-1-5

(9) Dr Duke’s Phytochemical and Ethnobotanical Databases  http://www.ars-grin.gov/duke/index.html

(10) CU JIAN-QIN, ZHONG JZ and PAR P (1990) GCMs analysis of the essential oil of celery seed. Indian Perfumer. 34(1–4), vi-vii.

(11) Grieve, M. A Modern Herbal. 1931. Jonathan Cape Ltd, London.

(12) Duke, J.A. The Green Pharmacy. Herbal remedies for common diseases and conditions. Rodale International Ltd; New edition edition (3 Jan 2003)

(13) Higdon, J. and Drake, V.J.  An Evidence-based Approach to Phytochemicals and Other Dietary Factors. Linus Pauling Institute,  Hardcover (2013), 2nd Edition, 368 pp. http://lpi.oregonstate.edu/books.html

(14) Ma X, He D, Ru X, Chen Y, Cai Y, Bruce IC, Xia Q, Yao X, Jin J. Apigenin, a plant-derived flavone, activates transient receptor potential vanilloid 4 cation channel. Br J Pharmacol. 2012 May;166(1):349-58. doi: 10.1111/j.1476-5381.2011.01767.x. PubMed PMID: 22049911; PubMed Central PMCID: PMC3415659.

(15) Moghadam MH, Imenshahidi M, Mohajeri SA. Antihypertensive effect of celery seed on rat blood pressure in chronic administration. J Med Food. 2013 Jun;16(6):558-63. doi: 10.1089/jmf.2012.2664. Epub 2013 Jun 4. PubMed PMID: 23735001; PubMed Central PMCID: PMC3684138.

(16) Le QT, Elliott WJ. Hypotensive and hypocholesterolemic effects of celery oil may be due to BuPh. Clin Res.1991;39:173A.

(17) Tsi D, Tan BKH. Cardiovascular pharmacology of 3-n-butylphthalide in spontaneously hypertensive rats. Phytotherapy Research. 1997;11:576-582.

(18) Ma X, He D, Ru X, Chen Y, Cai Y, Bruce IC, Xia Q, Yao X, Jin J. Apigenin, a plant-derived flavone, activates transient receptor potential vanilloid 4 cation channel. Br J Pharmacol. 2012 May;166(1):349-58. doi: 10.1111/j.1476-5381.2011.01767.x. PubMed PMID: 22049911; PubMed Central PMCID: PMC3415659.

(19) Le QT, Elliott WJ. Dose-response relationship of blood pressure and serum cholesterol to 3-n-butylphthalide, a component of celery oil. Clin Res. 1991;39:750A.

(20) Mimura Y, Kobayashi S, Naitoh T, Kimura I, Kimura M. The structure-activity relationship between synthetic butylidenephthalide derivatives regarding the competence and progression of inhibition in primary cultures proliferation of mouse aorta smooth muscle cells. Biol Pharm Bull. 1995;18(9):1203-1206.

(21) Yu SR, Gao NN, Li LL, Wang ZY, Chen Y, Wang WN. The protective effect of 3-butyl phthalide on rat brain cells. Yao Hsueh Hsueh Pao. 1988;23(9):656-661.

(22) Iyer D, Patil UK. Effect of chloroform and aqueous basic fraction of ethanolic extract from Apium graveolens L. in experimentally-induced hyperlipidemia in rats. J Complement Integr Med. 2011 Sep 27;8. doi:pii: /j/jcim.2011.8.issue-1/1553-3840.1529/1553-3840.1529.xml. 10.2202/1553-3840.1529. PubMed PMID: 22718672.

(23) Lewis, D.A.; Tharib, S.M.; Bryan, G.; Veitch, A. Pharmaceutical Biology, 1985, Vol. 23, No. 1 : Pages 27-32. The Anti-inflammatory Activity of Celery Apium graveolens L. (Fam. Umbelliferae) (doi: 10.3109/13880208509070685)

(24) Al-Hindawi MK, Al-Deen IH, Nabi MH, Ismail MA. Anti-inflammatory activity of some Iraqi plants using intact rats. J Ethnopharmacol. 1989 Sep;26(2):163-8. PubMed PMID: 2601356.

(25) Mencherini T, Cau A, Bianco G, Della Loggia R, Aquino RP, Autore G. An extract of Apium graveolens var. dulce leaves: structure of the major constituent, apiin, and its anti-inflammatory properties. J Pharm Pharmacol. 2007 Jun;59(6):891-7. PubMed PMID: 17637182.

(26) Ziyan L, Yongmei Z, Nan Z, Ning T, Baolin L. Evaluation of the anti-inflammatory activity of luteolin in experimental animal models.Planta Med. 2007 Mar;73(3):221-6. Epub 2007 Mar 12. PubMed PMID: 17354164.

(27) Christensen LP, Brandt K. Bioactive polyacetylenes in food plants of the Apiaceae family: occurrence, bioactivity and analysis. J Pharm Biomed Anal. 2006 Jun 7;41(3):683-93. Epub 2006 Mar 7. Review. PubMed PMID: 16520011.

(28) Ren S, Lien EJ. Natural products and their derivatives as cancer chemopreventive agents. Prog Drug Res. 1997;48:147-71. Review. PubMed PMID: 9204686.

(29) López-Lázaro M. Distribution and biological activities of the flavonoid luteolin. Mini Rev Med Chem. 2009 Jan;9(1):31-59. Review. PubMed PMID: 19149659.

(30) Lim do Y, Jeong Y, Tyner AL, Park JH. Induction of cell cycle arrest and apoptosis in HT-29 human colon cancer cells by the dietary compound luteolin. Am J Physiol Gastrointest Liver Physiol. 2007 Jan;292(1):G66-75. Epub 2006 Aug 10. PubMed PMID: 16901994.

(31) Meeran SM, Katiyar SK. Cell cycle control as a basis for cancer chemoprevention through dietary agents. Front Biosci. 2008 Jan 1;13:2191-202. Review. PubMed PMID: 17981702; PubMed Central PMCID: PMC2387048.

(32) Sultana S, Ahmed S, Jahangir T, Sharma S. Inhibitory effect of celery seeds extract on chemically induced hepatocarcinogenesis: modulation of cell proliferation, metabolism and altered hepatic foci development. Cancer Lett. 2005 Apr 18;221(1):11-20. PubMed PMID: 15797622.

(33) Madkour NK. The beneficial role of celery oil in lowering of di(2-ethylhexyl) phthalate-induced testicular damage. Toxicol Ind Health. 2012 Nov 16. [Epub ahead of print] PubMed PMID: 23160384.

(34) Baananou S, Bouftira I, Mahmoud A, Boukef K, Marongiu B, Boughattas NA. Antiulcerogenic and antibacterial activities of Apium graveolens essential oil and extract. Nat Prod Res. 2013 Jun;27(12):1075-83. doi: 10.1080/14786419.2012.717284. Epub 2012 Aug 30. PubMed PMID: 22934666.

(35) Al-Howiriny T, Alsheikh A, Alqasoumi S, Al-Yahya M, ElTahir K, Rafatullah S. Gastric antiulcer, antisecretory and cytoprotective properties of celery (Apium graveolens) in rats. Pharm Biol. 2010 Jul;48(7):786-93. doi: 10.3109/13880200903280026. PubMed PMID: 20645778.

(36) Carlsen MH, Halvorsen BL, Holte K, Bøhn SK, Dragland S, Sampson L, Willey C, Senoo H, Umezono Y, Sanada C, Barikmo I, Berhe N, Willett WC, Phillips KM, Jacobs DR Jr, Blomhoff R. The total antioxidant content of more than 3100 foods, beverages, spices, herbs and supplements used worldwide. Nutr J. 2010 Jan 22;9:3. doi: 10.1186/1475-2891-9-3. PubMed PMID: 20096093; PubMed Central PMCID: PMC2841576.

(37) Zhou Y, Taylor B, Smith TJ, Liu ZP, Clench M, Davies NW, Rainsford KD. A novel compound from celery seed with a bactericidal effect against Helicobacter pylori. J Pharm Pharmacol. 2009 Aug;61(8):1067-77. doi: 10.1211/jpp/61.08.0011. PubMed PMID: 19703351.

(38) Rani P, Khullar N. Antimicrobial evaluation of some medicinal plants for their anti-enteric potential against multi-drug resistant Salmonella typhi. Phytother Res. 2004 Aug;18(8):670-3. PubMed PMID: 15476301.

(39) Peng Y, Sun J, Hon S, Nylander AN, Xia W, Feng Y, Wang X, Lemere CA. L-3-n-butylphthalide improves cognitive impairment and reduces amyloid-beta in a transgenic model of Alzheimer’s disease. J Neurosci. 2010 Jun 16;30(24):8180-9. doi: 10.1523/JNEUROSCI.0340-10.2010. PubMed PMID: 20554868.

(40) Peng Y, Hu Y, Xu S, Li P, Li J, Lu L, Yang H, Feng N, Wang L, Wang X. L-3-n-butylphthalide reduces tau phosphorylation and improves cognitive deficits in AβPP/PS1-Alzheimer’s transgenic mice. J Alzheimers Dis. 2012;29(2):379-91. doi: 10.3233/JAD-2011-111577. PubMed PMID: 22233765.

(41) Tafreshi AP, Ahmadi A, Ghaffarpur M, Mostafavi H, Rezaeizadeh H, Minaie B, Faghihzadeh S, Naseri M. An Iranian herbal-marine medicine, MS14, ameliorates experimental allergic encephalomyelitis. Phytother Res. 2008 Aug;22(8):1083-6. doi: 10.1002/ptr.2459. PubMed PMID: 18570265.

(42) Mark Douglas Hill. The Aphrodisiac Encycopedia – a compendium of culinary come-ons. Square Peg, 6 October 2011.

(43) Claus R, Hoppen HO. The boar-pheromone steroid identified in vegetables. Experientia. 1979 Dec 15;35(12):1674-5. PubMed PMID: 520500.

(44) Wysocki CJ, Beauchamp GK. Ability to smell androstenone is genetically determined. Proc Natl Acad Sci U S A. 1984 Aug;81(15):4899-902. PubMed PMID: 6589634; PubMed Central PMCID: PMC391599.

(45) Domeena C. Renshaw, MD.  Aphrodisiacs: The Science and the Myth  JAMA. 1986;255(1):98-99. doi:10.1001/jama.1986.03370010108037

(46) Alan Crozier, Michael N. Clifford, Hiroshi Ashihara (Editors). Plant Secondary Metabolites: Occurrence, Structure and Role in the Human Diet. Wiley Online Library. Published Online: 12 NOV 2007; Print ISBN: 9781405125093; Online ISBN: 9780470988558; DOI: 10.1002/9780470988558

(47) Deleo VA. Photocontact dermatitis. Dermatol Ther. 2004;17(4):279-88. Review. PubMed PMID: 15327473.

(48) Gadermaier G, Hauser M, Egger M, Ferrara R, Briza P, Santos KS, Zennaro D, Girbl T, Zuidmeer-Jongejan L, Mari A, Ferreira F. Sensitization prevalence, antibody cross-reactivity and immunogenic peptide profile of Api g 2, the non-specific lipid transfer protein 1 of celery. PLoS One. 2011;6(8):e24150. doi: 10.1371/journal.pone.0024150. Epub 2011 Aug 29. PubMed PMID: 21897872; PubMed Central PMCID: PMC3163685.

(49) Brijesh K. Tiwari (Editor), Nigel P. Brunton (Editor), Charles Brennan (Editor). Handbook of Plant Food Phytochemicals: Sources, Stability and Extraction [Hardcover]. Wiley-Blackwell (22 Feb 2013)

(50) Jiménez-Monreal AM, García-Diz L, Martínez-Tomé M, Mariscal M, Murcia MA. Influence of cooking methods on antioxidant activity of vegetables. J Food Sci. 2009 Apr;74(3):H97-H103. doi: 10.1111/j.1750-3841.2009.01091.x. PubMed PMID: 19397724.

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Angelina Jolie, cancer, your genes and your fate

Angelina-Jolie-1

Angelina Jolie

It must have taken courage for Angelina Jolie to tell the world, via an article in the New York Times, that she had undergone a preventive double mastectomy.  A-list actresses are usually judged on their body image as much as on their acting ability.

Angelina made this choice because her doctors had warned her that she has an 87% risk of developing breast cancer and a 50% risk of getting ovarian cancer because her mother died of breast cancer and she carries the BRCA1 gene.

I respect Angelina for making a choice which felt right for her and her family.

That is all any of us can do when faced with difficult decisions and the tsunami of judgement that has greeted her article is regrettable.

The story does, however, raise fascinating questions about whether we are really at the mercy of our genes.

Do our genes dictate our fate or do we have any power over them?

I want to tell you what I think and why.

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In 1868, Friedrich Miescher discovered the presence of DNA, and in 1953, James Watson and Francis Crick discovered its molecular structure, with the help of Maurice Wilkins, Rosalind Franklin, Erwin Chargaff and Linus Pauling.

DNA Watson and Crick

In the years that followed, scientists have learned a great deal about how this genetic code dictates who we are.

Our DNA – specifically the 25,000 genes identified by the Human Genome Project – is now widely regarded as the instruction book for the human body.

Genetic science has attracted billions of dollars of research funding and was heralded as the key to understanding and curing diseases like cancer.

The trouble is that despite all the money that has been poured into it, our knowledge of genetics has not yielded the promised revolutionary cures for cancer on a widespread scale.

Whilst the latest official report on the “War on Cancer” from America indicates that death rates for all cancers combined decreased by 1.5 percent per year from 2000 to 2009 [1], this is no greater than the previous five year period.

Deaths are still rising for certain cancer types including liver, pancreatic, uterus and, among men, melanoma.  Rates of human papillomavirus (HPV)–related cancers, such as oral, anal, vaginal, vulval, penis and cervical, also remain stubbornly high despite the availability of a vaccine.  And many epithelial cancers (carcinomas) and effectively all mesenchymal cancers (sarcomas) remain incurable.

There were decreases in new breast cancer cases about a decade ago, as many women stopped using hormone therapy after menopause.  Since then, overall breast cancer incidence has reached a plateau, and rates have increased among black women.

The decrease in cancer mortality is driven largely by the decrease in cancer incidence, which is mostly because of the decrease in smoking [1]. Smoking can cause more than a dozen cancers, including lung, head, neck, bladder and mouth.

smoking addiction

Although improvements in screening and treatment for breast and some other cancers have cut death rates, most of the expensive new drugs prolong survival for no more than three or four months on average.

James Watson, famous for his part in the discovery of the structure of DNA, wrote in a recent edition of the Royal Society Journal “Open Biology”[2]:

Even though an increasing variety of intelligently designed, gene-targeted drugs now are in clinical use, they generally only temporarily hold back the fatal ravages of major cancers such as those of the lung, colon and breast that have become metastatic and gone beyond the reach of the skilled surgeon or radiotherapist.  Even though we will soon have comprehensive views of how most cancers arise and function at the genetic and biochemical level, their ‘curing’ seems now to many seasoned scientists an even more daunting objective than when the ‘War on Cancer’ was started by President Nixon in December 1971.

When we look at the decades of investments, the cost of treatments, the number of researchers and journals, and at the number of people who continue to die, we have to ask if we are barking up the wrong tree.

I believe we are.

The reality is that as fast as scientists find a ‘magic bullet’ to block a particular protein or cellular pathway to decimate cancer cells, the cancer cells find a way to circumvent the therapy, thrive and proliferate.

How do they do this?

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Well it turns out that DNA, the genome, is only half the story.

This should not be a surprise given that chromosomes contain only 50 per cent DNA; the other 50 per cent is protein.

Within each chromosome, DNA is wrapped around proteins called histones.  Both DNA and histones are covered in millions of tiny chemical tags.

This second layer of structure comprising histones and chemical tags is called the epigenome – meaning literally “above the genome”.

The epigenome shapes the physical structure of the genome, the DNA.  It tightly wraps inactive genes making them unreadable.  It relaxes around active genes making them easily accessible.

Epigenome

Epigenome

Different sets of genes are active in different cell types.

A human liver cell, for example, contains the same DNA as a brain cell, yet somehow it knows to code only those proteins needed for the functioning of the liver.  Those instructions are found not in the letters of the DNA itself but on the array of chemical tags which are part of the epigenome.

The DNA code remains fixed for life but the epigenome is flexible.

Epigenetic tags react to signals within the cell environment and to signals from the outside environment, such as diet, stress and our thoughts.

The epigenome adjusts the expression of specific genes in response to our rapidly changing environment.

How does this work?

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In the 1980s, researchers discovered that the answer to this question lay in specific chemical modifications to genomic DNA and its associated histone proteins, without changing the DNA itself at all.

What are these modifications?

In school biology lessons we learn that DNA is built from four different units called nucleotides: adenine, cytosine, guanine, and thymine.

In one type of epigenetic modification, a methyl group (one carbon atom linked to three hydrogen atoms -CH3) is added to specific cytosine bases of the DNA with help from enzymes.

Microsoft PowerPoint - Presentation1 (3) [Read-Only]

DNA methylation. Credit: Adrian Bird

This process, called DNA methylation, is known to play a key role in both development and disease.

Methylation of DNA affects the way the molecule is shaped and, consequently, regulates which genes are available to be ‘read’ or transcribed.

Recently, another type of epigenetic modification of DNA was discovered: the addition of a hydroxymethyl group (–CH2–OH) to specific cytosine bases of DNA.

Histone proteins can also be modified in a number of ways; in addition to methylation, they can be modified with acetyl groups (acetylation), phosphate groups (phosphorylation), ubiquitin proteins (ubiquitylation), and SUMO proteins (sumoylation).

But epigenetic phenomena are not restricted to DNA methylation and various types of histone modifications.

Scientists have found that RNA molecules themselves can also regulate DNA directly by physically blocking or influencing the reading of DNA sequences.

These RNA molecules aren’t the classic messenger RNA (mRNA) molecules we learn about in school biology that carry the information from DNA in the nucleus to the cytoplasm of a cell.  Rather, these RNA molecules – called antisense RNAs, microRNAs, and noncoding RNAs – stay primarily within the nucleus, where they induce changes in DNA function.

It is not yet fully understood how these RNA molecules work but it appears they may bind to histone proteins and/or help to turn off gene promoters.

So how does the environment interact with the epigenome and influence our genes?

dividing line

One of the most exciting discoveries of modern science is that our DNA, the genome, responds dynamically to the environment.

Stress, diet, behaviour, toxins and other factors activate the chemical tags or switches that turn our genes on and off.

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Nutrition is one of the easier environmental factors to study with respect to epigenetic changes and is receiving considerable research effort.

One of the most stunning examples of the effect of nutrition on gene expression was an experiment conducted at Duke University in 2000 [3].

Randy Jirtle and his postdoctoral student Robert Waterland took pairs of fat, yellow mice which carry the agouti gene, which is also found in humans.  This gene makes the rats extremely hungry and renders them prone to obesity, diabetes and cancer.

agoutimice

Typically, when agouti mice breed, most of the offspring are identical to the parents: yellow, fat and susceptible to disease.

In this experiment, the researchers simply changed the diet of the mothers.

Before conception and during pregnancy, one set of mice were fed a diet containing nutrients rich in methyl groups, for example, folate and the B vitamins.  These molecules are found in many plant foods and in supplements given to pregnant women.  The other set of genetically identical mice were fed a regular diet low in these nutrients over the same time period.

Mice with the agouti gene (picture from University of Utah)

Mice with the agouti gene (picture from University of Utah)

To the researchers’ amazement, the mothers fed the methyl rich diet produced brown, slim, healthy offspring, whereas the mothers on the normal diet produced the typical yellow, fat and sickly offspring.  The only difference between the two was the diet the mothers were given.

Methyl groups from the dietary supplements (folic acid, vitamin B12, choline, and betaine) bound to the DNA of the mice, increasing DNA methylation and preventing the agouti gene from being expressed.

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Chemicals and additives that enter our bodies can also affect the epigenome.

Bisphenol A (BPA) is a compound used to make polycarbonate plastic.  It is in many consumer products including water bottles and the lining of tin cans.

When pregnant yellow agouti mothers were fed BPA, more yellow, unhealthy babies were born than normal.  Exposure to BPA during early development had caused decreased methylation of the agouti gene.

However, when BPA-exposed, pregnant yellow mice were fed a diet containing B vitamins, folate, choline and betaine, which are rich in methyl groups, the offspring were predominantly brown.  The maternal nutrient supplementation had counteracted the negative effects of exposure to a genotoxic chemical [4].

Mice with the agouti gene

Mice with the agouti gene fed with Bisphenol A

The father’s diet may be important too.

A Swedish paper published in 2007 [5] provided evidence from historical records that a shortage of food for grandfathers was associated with extended lifespan of their grandchildren.  Food abundance, on the other hand, was associated with a greatly shortened lifespan of the grandchildren due to diabetes and heart disease.

This suggests the possibility that during this critical period of development for the grandfather, epigenetic mechanisms are “capturing” nutritional information about the environment to pass on to the next generation.

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Honey bees, too, provide a beautiful example of the power of nutrition over gene expression.

The larvae that develop into workers and queens are genetically identical.  Larvae destined to become queens, however, are fed a diet of royal jelly in a special compartment in the hive called a queen cup.

Queen cup

Queen cup

Royal jelly is a complex, protein-rich substance secreted from glands on the heads of worker bees.   Consumption of royal jelly enables the queen to develop functional ovaries and a larger abdomen for egg laying, while worker bees remain sterile.

The queen also develops different behaviours from those of the workers, becoming more aggressive, looking for mates and communicating using sounds.  The queen is fed royal jelly exclusively for the rest of her life.

In a recent series of experiments, scientists determined that royal jelly silences a key gene (Dnmt3), which codes for an enzyme involved in genome-wide gene silencing [6].  When Dnmt3 is active in bee larvae, the queen genes are epigenetically silenced and the larvae develop into the default “worker” variety.  But when royal jelly turns Dnmt3 off, certain genes jump into action that turn the larvae into queens.

This is all very interesting but how is it relevant to cancer?

dividing line

Cancer develops when a cell becomes abnormal and begins to grow out of control.

Normal cells and cancer cells

Normal cells and cancer cells (picture from University of Utah)

Cancer can begin when a mutation changes a cell’s DNA sequence.  We know that mutations in at least several hundred human genes (out of a total of 25 000 genes) can lead to the abnormal cell growth and division process that generates human cancer [7].

But cancer cells also have abnormal epigenomes.

In many cancers, some genes are turned up and some are turned down – often in the same cells.  Cancer is just one in a growing number of diseases that are being linked to changes in the epigenome.

Some cancer cells have a lower level of methylation (more active DNA) than healthy cells.

less methyl - genes on

Too little methylation causes:

  • activation of genes that promote cell growth
  • chromosome instability – highly active DNA is more likely to be duplicated, deleted and moved to other locations
  • loss of imprinting.  For most genes, we inherit two working copies – one from each parent. But with imprinted genes, we inherit only one working copy. Depending on the gene, either the copy from your mother or your father is epigenetically silenced.  Silencing usually happens through the addition of methyl groups during egg or sperm formation.

Cancer cells can also have genes that have more methyl (are less active) than normal.

More methylation - genes off (picture from University of Utah)

The types of genes that are turned down in cancer cells:

  • keep cell growth in check
  • repair damaged DNA
  • initiate programmed cell death

But here is the real magic.

Unlike mutations, DNA methylation and histone modifications are reversible.

Researchers are thus exploring drug therapies that can change the epigenetic profiles of cancer cells.  One challenge with epigenetic therapies is figuring out how to target drugs to the right genes in the right tissues.

It is for example possible to reactivate dormant tumour-suppressor genes with drugs which remove methyl groups from histone proteins [8].

DNA demethylating drugs in low doses have clinical activity against some tumours, for example, leukaemia, but have not yet been shown to have activity against solid tumours [9].

A key problem is that these demethylating agents are non-specific, often toxic and can potentially exert their effects in healthy tissues paradoxically causing new tumours to develop.

Other drugs targeted at the epigenome are the histone deacetylase (HDAC) inhibitors.

These can induce differentiation, cell-cycle arrest, and programmed cell death (apoptosis) in vitro, although it has not been possible to pinpoint a specific mechanism that explains these effects [10].

In clinical trials, HDAC inhibitors are associated with a low incidence of adverse events.  The first drug of this type, suberoylanilide hydroxamic acid (vorinostat),has been approved by the Food and Drug Administration for the treatment of cutaneous T-cell lymphoma [11].  The efficacy of HDAC inhibitors in the treatment of other tumours is limited.

Research on manipulating specific targets in the epigenome with drugs is, in my view, likely to be as doomed to failure as the decades of research looking for drugs which target the genome.

This is because complex biological systems like the human body operate through a large number of simultaneous reactions occurring in a highly integrated and concerted manner.

The body has multiple back-up systems in case one system is bypassed.

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Nutrition, epigenetics and cancer

In addition to drug research, there is also considerable interest in the way nutrients affect the epigenome in relation to cancer [12] [13] [14] [15].

Extensive review of the highest quality papers in the scientific literature by a team of international experts on behalf of the World Cancer Research Fund has led to the view that at least 30-40 per cent of cancers potentially can be avoided through dietary modification [16].

Many bioactive components have been identified in food, which are protective at different stages of cancer formation.  Diet has been implicated in many pathways involved in carcinogenesis, including apoptosis, cell cycle control, differentiation, inflammation, angiogenesis, DNA repair, and carcinogen metabolism [12].  These are also processes likely to be regulated by DNA methylation and other epigenetic events.

A host of bioactive substances in the diet, from alcohol to zinc, have been shown to modulate DNA methylation and cancer susceptibility [12] [16].

Dietary factors that are involved in one-carbon metabolism provide the most compelling data for the interaction of nutrients and DNA methylation because they influence the supply of methyl groups and therefore the biochemical pathways of methylation processes. These nutrients include vitamin B12, vitamin B6, folate, methionine, and choline.

b-vitamin

A large number of epidemiologic and clinical studies suggest that dietary folate intake and blood folate concentrations are inversely associated with colorectal cancer risk [17].

Alcohol consumption increases breast cancer incidence by 41 percent for women consuming 30-60 g/day alcohol compared to non-drinking women [18].  Alcohol consumption has been shown to alter folate metabolism and increase cancer susceptibility [19] [20].

adults drinking

Sulforaphanes from broccoli, diallyl disuphides from garlic and resveratrol in wine, have been shown (in vitro and in vivo) to alter epigenetic processes with positive consequences for cell function, including control of proliferation, upregulated apoptosis and a reduction in inflammation [21].

broccoli

Green tea polyphenols have been shown to inhibit carcinogenesis through effects on DNA methylation in many animal models [22].

green tea

Soy phytoestrogens, such as genistein, have been shown to prevent certain mammary and prostate cancers via protective DNA methylation [12].

Apigenin in parsley, curcumin in turmeric, and coffee polyphenols are reported to inhibit DNA methyltransferase enzyme activity in various cancer models [23] [24].

soy turmeric parsley

Zinc deficiency, selenium deficiency and vitamin A excess have been associated with DNA hypomethylation in rat liver, whilst vitamin C deficiency caused hypermethylation in lung cancer cells [12].

There are many more examples but these few serve to illustrate the fact that many dietary components interact in a complex and dynamic manner with the epigenome to alter gene expression and susceptibility to cancer and other diseases.

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Whilst studying the effect of individual nutrients on epigenetic processes is instructive, it is far too simplistic.  Food contains an extraordinary array of nutrients and other substances that work together in concert to create health or disease.

china study

Professor T. Colin Campbell’s thought-provoking book “The China Study” opened up the scientific literature on the effect of diet on health to a wide audience.  He explained the evidence showing that a plant-based diet is the healthiest way to eat, dramatically reducing the risk of a range of chronic diseases, such as arthritis, diabetes, heart disease and many cancers.

This dietary effect is due to the consumption of myriad beneficial substances found in whole plant foods, which interact with the epigenome to ensure that our genes are switched on and off correctly. 

Colin Campbell expands on this theme in his new book “Whole: Rethinking the Science of Nutrition”, due out on 23 May 2013.  He argues that nutritional science, long stuck in a reductionist mindset, is at the cusp of a revolution.  He writes:

The traditional “gold standard” of nutrition research has been to study one chemical at a time in an attempt to determine its particular impact on the human body. These sorts of studies are helpful to food companies trying to prove there is a chemical in milk or pre-packaged dinners that is “good” for us, but they provide little insight into the complexity of what actually happens in our bodies or how those chemicals contribute to our health.

Diet is, however, only one of many environmental influences on the way our genes behave.

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There is also a growing body of scientific research surfacing from the medical literature showing that our thoughts and emotions directly affect expression of our genes.

Mind over Medicine Lissa Rankin

Lissa Rankin MD’s new book “Mind over Medicine” is an excellent and readable synopsis of some of the key studies in this area and is thoroughly recommended.

David Hamilton PhD is an organic chemist who used to work in pharmaceutical research inventing drugs for cardiovascular disease.  He left his job because he became more interested in the placebo effect than the effect of drugs he was trying to invent.  David has also written some fascinating books on the science of how the mind affects the body, including “How Your Mind Can Heal Your Body”.

Bruce Lipton PhD, a developmental cell biologist and former Professor of Anatomy at University of Wisconsin School of Medicine, was one of the original researchers in the field of epigenetics and opened my eyes to its exciting advances in his book “The Biology of Belief”.

Dean Ornish MD, Clinical Professor of Medicine at the University of California, San Francisco, has been actively researching the effects of lifestyle factors, including diet, thoughts, social interactions and love, on cancer and other diseases for over 35 years.

The research that he and his colleagues conducted has been published in the Journal of the American Medical Association, The Lancet, Proceedings of the National Academy of Sciences, Circulation, The New England Journal of Medicine, the American Journal of Cardiology, The Lancet Oncology, and elsewhere.

research-journals

This research is not pseudoscience woo-woo.  It is high quality, properly designed and controlled, peer-reviewed science published in some of the most prestigious medical journals in the world.  And it is only the tip of the iceberg.

The knowledge and understanding we are gaining from modern scientific research in the field of epigenetics has profound implications.

It demonstrates that we do not have to be the victims of our genes.

Genes may predispose us to certain health conditions but their presence does not inevitably determine our health outcomes.

Our environment and lifestyle choices – the thoughts we think, the food and drink we consume, our physical activity, whether or not we smoke, our relationships, our work, our finances, our level of stress, our stewardship of the earth – all interact with our genes to determine our fate.

The truth is that all of us will die one day.

While we are here, though, it is about having a life, not just living.

So embrace your power, trust your instincts about what is best for you, and do not allow fear-mongers on both sides of controversial debates, like the one about Angelina Jolie, scare you to death.

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References

[1] Jemal, A. et al (2013).  Annual Report to the Nation on the Status of Cancer, 1975–2009, Featuring the Burden and Trends in Human Papillomavirus (HPV)–Associated Cancers and HPV Vaccination Coverage Levels.  JNCI J Natl Cancer Inst (2013) doi: 10.1093/jnci/djs491 First published online: January 7, 2013

http://m.jnci.oxfordjournals.org/content/early/2013/01/03/jnci.djs491.full

[2] Watson, J.  Oxidants, antioxidants and the current incurability of metastatic cancers.  Open Biol. 2013 3, 120144, published online 8 January 2013

[3] Waterland RA, Jirtle RL. Transposable elements: targets for early nutritional effects on epigenetic gene regulation. Mol Cell Biol 2003;23(15):5293–5300

[4] Dolinoy D.C., Huang D., Jirtle R.L. (2007). Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. PNAS, 104: 13056-13061.

[5] Kaati G., Bygren L.O., Pembrey M., Sjostrom M. (2007). Transgenerational response to nutrition, early life circumstances and longevity. European Journal of Human Genetics, 15: 784-790.

[6] Kucharski R., Maleszka J., Foret S., Maleszka R. Nutritional Control of Reproductive Status in Honeybees via DNA Methylation (2008). Science, 319: 1827-1830 (registration required).

[7] Jones S, Vogelstein B, Velculescu VE, Kinzler KW. 2008 Core signaling pathways in human pancreatic cancers revealed by global genomic analyses. Science 321, 1801. (doi:10.1126/science.1164368)

[8] Esteller, M.  Epigenetics in cancer.  N Engl J Med 2008;358:1148-59.

[9] Mack GS. Epigenetic cancer therapy makes headway. J Natl Cancer Inst 2006; 98:1443-4.

[10] Bolden JE, Peart MJ, Johnstone RW.Anticancer activities of histone deacetylase inhibitors. Nat Rev Drug Discov 2006;5:769-84.

[11] Marks PA, Breslow R. Dimethyl sulfoxide to vorinostat: development of this histone deacetylase inhibitor as an anticancer drug. Nat Biotechnol 2007;25:84-90.

[12] Davis, C.D and Uthus, E.O. DNA Methylation, Cancer Susceptibility and Nutrient Interactions. Exp Biol Med November 2004 vol. 229 no. 10, 988-995

[13] Khan, S.I. et al (2012). Epigenetic Events Associated with Breast Cancer and Their Prevention by Dietary Components Targeting the Epigenome. Chem. Res. Toxicol. 2012, 25, 61–73

[14] Liu, L. Et al. Aging, cancer and nutrition: the DNA methylation connection. Mechanisms of Ageing and Development Volume 124, Issues 10–12, December 2003, Pages 989–998

[15] Su, L.J. et al.  Epigenetic contributions to the relationship between cancer and dietary intake of nutrients, bioactive food components, and environmental toxicants. Frontiers in Genetics, Vol 2, Article 91, 1-12,, 09 January 2012 | doi: 10.3389/fgene.2011.00091

[16] World Cancer Research Organisation. 2nd Expert Report: Food, Nutrition, Physical Activity and the Prevention of Cancer: A Global Perspective. Washington DC: AICR, 2007. http://www.dietandcancerreport.org/expert_report/report_contents/index.php

[17] Kim Y.-I.  Folate and DNA methylation: a mechanistic link between folate deficiency and colorectal cancer? Cancer Epidemiol Biomarkers Prev 13:511–519, 2004.

[18] Smith-Warner, S.A. et al.  Alcohol and breast cancer in women.  A pooled analysis of cohort studies.  JAMA 279 (1998), 535-540.

[19] van Engeland M, Weijenberg MP, Roemen GM, Brink M, de Bruine AP, Goldbohm RA, van den Brandt PA, Baylin SB, de Goeij AF, Herman JG. Effects of dietary folate and alcohol intake on promoter methylation in sporadic colorectal cancer: the Netherlands cohort study on diet and cancer. Cancer Res 63:3133–3137, 2003

[20] Choi SW, Stickel F, Baik HW, Kim YI, Seitz HK, Mason JB. Chronic alcohol consumption induces genomic but not p53-specific DNA hypomethylation in rat colon. J Nutr 129:1945–1950, 1999.

[21] Ross SA, Dwyer J, Umar A et al. (2008) Diet, epigenetic events and cancer prevention. Nutr Rev 66 (Suppl. 1), S1–S6.

[22] Fang MZ, Wang Y, Ai N, Hou Z, Sun Y, Lu H, Welsh W, Yang CS. Tea polyphenol (-)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer celllines. Cancer Res 63:7563–7570, 2003.

[23] Meeran, S. M., Ahmed, A., and Tollefsbol, T. O. (2010) Epigenetic targets of bioactive dietary components for cancer prevention and therapy. Clin. Epigenetics 1, 101–116.

[24] Lee, W. J., and Zhu, B. T. (2006) Inhibition of DNA methylation by caffeic acid and chlorogenic acid, two common catechol-containing coffee polyphenols. Carcinogenesis 27, 269–277.

How to prevent cancer

Vegetables and FruitsSix years ago the World Cancer Research Fund and the American Institute of Cancer Research published the mother of all literature reviews on food, nutrition, physical activity and the prevention of cancer (1).

A panel of 21 world-renowned scientists reviewed the research evidence and drew conclusions based on in-depth analysis of over 7,000 scientific studies published on cancer prevention over the last 50 years.

As a result of this review they made a number of recommendations:

  1. Be as lean as possible without becoming underweight
  2. Be physically active for at least 30 minutes per day
  3. Limit consumption of energy-dense foods and avoid sugary drinks
  4. Eat more of a variety of vegetables, fruit, whole grains and pulses
  5. Limit consumption of red meats and avoid processed meats
  6. If consumed at all, limit alcoholic drinks to 2 per day for men and 1 per day for women
  7. Limit consumption of salty foods and foods processed with salt
  8. Don’t use supplements to protect against cancer
  9. Do not smoke or chew tobacco
  10. Breastfeed exclusively for up to 6 months and then add other liquids and foods
  11. After treatment, cancer survivors should follow the recommendations for cancer prevention.

Since then further research has been conducted to see whether compliance with these recommendations has any effect on the risk of death from cancer and other diseases.

The findings were published in the American Journal of Clinical Nutrition on 3 April 2013 (2).

Researchers investigated nearly 380,000 people in nine European countries over 12 years and examined their diet and lifestyle to see how closely they complied with seven of World Cancer Research Fund/American Institute for Cancer Research’s (WCRF/AICR) Recommendations for Cancer Prevention.

They found that the risk of dying from several diseases, including cancer, circulatory diseases and respiratory diseases, can be reduced by 34 per cent if these recommendations are followed.

Those who most closely followed the WCRF/AICR Recommendations had a 50 per cent reduced chance of dying from respiratory disease, 44 per cent for circulatory disease and 20 per cent for cancer, when compared to the group with the lowest level of compliance.

The Recommendations with the greatest impact on reducing the risk of death from disease were being as lean as possible without becoming underweight (22 per cent reduced risk) and eating mostly plant foods (21 per cent).

In terms of cancer, limiting alcohol consumption and following the plant food recommendation reduced the risk of dying from the disease by the greatest margin, at 21 per cent and 17 per cent respectively.

The study is the first to examine breastfeeding as part of a combination of lifestyle changes to see what effect it has on risk of dying.  It showed that women who breastfed for at least six months had a reduced risk of death from cancer (ten per cent) and circulatory disease (17 per cent).

Although the WRCF/AICR recommendations were focused on the prevention of cancer, this study shows that adherence to these recommendations also reduces the risk of other diseases.

The bottom line is that maintaining a lean body by consuming a predominantly plant-based diet, being physically active and minimising intake of alcohol is most likely to protect you from cancer.  Looking after yourself in this way will also help to reduce your risk of circulatory and respiratory diseases.

If you would like to learn about how to introduce more plant-based dishes into your diet why not sign up for free email updates with information, recipes and news and visit my website at http://www.cookingforhealth.biz.

You can also stay in touch by joining me on Facebook and Twitter and LinkedIn.

References

1. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. Washington DC : AICR, 2007.

2. Adherence to the World Cancer Research Fund/American Institute for Cancer Research guidelines and risk of death in Europe: results from the European Prospective Investigation into Nutrition and Cancer cohort study. Anne-Claire Vergnaud et al. 3 April 2013, American Journal of Clinical Nutrition.

Towards a new paradigm for public health

Food-Vegetables-01In 1990, physician and health economist Christopher Murray at Harvard University and medical demographer Alan Lopez at the World Health Organisation embarked on the first ever attempt to measure the global burden of disease and developed the now-famous Disability Adjusted Life Year (DALY) metric that made it possible to combine estimates of mortality and morbidity burden around the world. DALY is the sum of years lived with disability [YLD] and years of life lost [YLL].

Since then, there have been estimates in 1999 to 2002 and 2004. But the latest iteration of the project, Global Burden of Disease 2010, has been on a different scale, involving nearly 500 researchers from more than 300 institutions in 50 countries. It is the largest ever systematic effort to describe the global distribution and causes of a wide array of major diseases, injuries, and health risk factors.

Twenty years ago, the project assessed the burden of 107 diseases and injuries and ten selected risk factors for the world and eight major regions over one calendar year. Now, thanks to advances in technology, the availability of data, and the participation of experts around the world, as well as the leadership of a core group of researchers, the scope has increased to 291 diseases and injuries in 21 regions, for 20 age groups, and an estimation of trends from 1990 to 2010. Global Burden of Disease 2010 also includes an assessment of 67 risk factors.

The results, published yesterday in seven articles in The Lancet, are set to shake up health priorities across the world.

In summary, the analysis shows that infectious diseases, maternal and child illness, and malnutrition now cause fewer deaths and less illness than they did twenty years ago. As a result, fewer children are dying every year, but more young and middle-aged adults are dying and suffering from disease and injury, as non-communicable diseases, such as cancer and heart disease, become the dominant causes of death and disability worldwide. Since 1970, men and women worldwide have gained slightly more than ten years of life expectancy overall, but they spend more years living with injury and illness.

There were 52.8 million deaths in 2010 compared with 46.5 million deaths in 1990. Of these, 12.9 million were from ischaemic heart disease and stroke, or one in four deaths worldwide, compared with one in five in 1990. Cancer claimed 8 million lives in 2010 compared with 5.8 million in 1990; trachea, bronchus and lung cancer accounted for 20% of these. Twice as many people died of diabetes in 2010 – 1.3. million – than in 1990, which is higher than deaths from tuberculosis or malaria (1.2 million each). Deaths from HIV/AIDS increased from 0.30 million in 1990 to 1.5 million in 2010, reaching a peak of 1.7 million in 2006. The fraction of global deaths due to injuries (5.1 million deaths) was marginally higher in 2010 (9.6%) compared with two decades earlier (8.8%). This was driven by a 46% rise in deaths worldwide due to road traffic accidents (1.3 million in 2010) and a rise in deaths from falls.

The contributions of risk factors to regional and global burden of diseases and injuries has shifted substantially between 1990 and 2010, from risk factors that mainly cause communicable diseases in children to risk factors that mainly cause non-communicable diseases in adults.

The proportion of overall disease burden attributable to childhood underweight – the leading risk factor worldwide in 1990 – had more than halved by 2010, making childhood underweight the eighth risk worldwide, behind six behavioural and physiological risks, and household air pollution from solid fuels. Other risks for child mortality, such as non-exclusive and discontinued breastfeeding, micronutrient deficiencies, and unimproved water and sanitation, have also fallen. However, child and maternal undernutrition risks collectively still account for almost 7% of disease burden in 2010, with unimproved water and sanitation accounting for almost 1%.

Of the non-communicable disease risks, high blood pressure, high body-mass index, high fasting plasma glucose, alcohol use, and dietary risks have increased in relative importance. This overall shift has arisen from a combination of the ageing population, substantial achievements in lowering mortality of children aged younger than 5 years, and changes in risk factor exposure.

These broad global patterns mask enormous regional variation in risks to health. In sub-Saharan Africa, risks such as childhood underweight, household air pollution from solid fuels, and suboptimal breastfeeding continue to cause a disproportionate amount of health burden, despite decreasing. The shift to risk factors for non-communicable disease was clear in east Asia, North Africa and Middle East, and Latin America.

For people aged 15 to 49 years, the leading risk factor worldwide was alcohol use, followed by tobacco smoking including second-hand smoke, high blood pressure, high body-mass index, diet low in fruits, drug use, and occupational risk factors for injuries. Risk factor rankings in this age group stayed broadly similar between 1990, and 2010, with the exception of iron deficiency, which dropped from the fourth leading risk factor in 1990, to ninth in 2010.

High blood pressure, tobacco smoking including second-hand smoke, alcohol use, and diet low in fruits were all in the top five risk factors for adults aged 50 to 69 years and adults older than 70 years, in both 1990, and 2010, accounting for a large proportion of disease burden in both age groups. Globally, high blood pressure accounted for more than 20% of all health loss in adults aged 70 years and older in 2010, and around 15% in those aged 50 to 69 years. Tobacco smoking including second-hand smoke accounted for more than 10% of global disease burden in each of these age groups in 2010.

Globally, the sum of years lived with disability and years of life lost (DALY), was influenced most by dietary risk factors and physical inactivity – together these were responsible for 10% of the global disease burden in 2010.

Of the individual dietary risk factors, the largest attributable burden in 2010 was associated with diets low in fruits (4.9 million deaths), followed by diets high in sodium (4.0 million deaths), low in nuts and seeds (2.5 million deaths), low in whole grains (1.7 million), low in vegetables (1.8 million deaths), and low in seafood omega-3 fatty acids (1.4 million deaths). Physical inactivity and low physical activity accounted for 3.2 million deaths.

This impressive analysis of global health issues by Christopher Murray and colleagues provides much reason for hope but also challenges the current medical paradigm and global healthcare system.

It shows clearly that the focus of global health authorities in recent decades on reducing infection and malnutrition has paid off – life expectancy has increased almost everywhere. This focus needs to continue to minimise incidence of diseases like tuberculosis, malaria and HIV/AIDs.

It also reveals, however, that the leading causes of death in the modern developed world are conditions which cannot be controlled by vaccinations, antibiotics, improved sanitation or insecticides. The data provide evidence that the risk factors for non-communicable diseases like heart disease, cancer and diabetes, are predominantly related to poor diet and lifestyle.

The large attributable burden for dietary risk factors such as diets low in fruits, vegetables, whole grains, nuts and seeds, and seafood omega-3 fatty acids might come as a surprise to some. The large burden is caused by both high exposure, e.g., low intake of fruits and vegetables in many regions – and large effect sizes.

Given the crucial role of dietary and lifestyle factors in determining long-term health, the answer to alleviating the suffering created by these chronic non-communicable diseases does not lie in the current medical model, with its preoccupation with drugs and surgery. Our doctors are trained to relieve symptoms not to address the underlying causes of chronic disease. Powerful commercial interests in the food, pharmaceutical and health sectors drown out the voices of those who can see that the solution is really very simple.

Widespread consumption of plant-based diets, rich in vegetables, fruit, whole grains, beans, nuts and seeds, together with not smoking and more physical activity, would transform people’s lives and radically reduce healthcare costs. It is not rocket science.

Dr Murray, I salute you and your colleagues for a first rate piece of work. May the truths you have exposed become part of mainstream understanding as quickly as possible and lead to a sea change in our approach to health and well-being.

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References

Murray et al (2012). Global Burden of Disease 2010. The Lancet, 13 December 2012.

Guest Blog – Nutrition and Cancer

Today my Guest Blogger is Jillian McKee, who has worked as the Complementary Medicine Advocate at the Mesothelioma Cancer Alliance since June 2009.  Bringing a wealth of personal and professional experience to the organization, Jillian spends most her time on outreach efforts and spreading information about the integration of complementary and alternative medicine when used in conjunction with traditional cancer treatment.

Jillian’s article is about the benefits of eating healthy during and after a diagnosis of any kind of cancer.

Why Cancer and Nutrition Go Hand-in-Hand

If you have recently been diagnosed with cancer, you are more than likely very distraught and aggravated.  Receiving this type of diagnosis is one of the most difficult things that anyone can hear from their doctor.  Thankfully, there is a way to improve your well-being while undergoing cancer treatment.  The best way to improve your life during this time is to incorporate proper nutrition into your daily routine.  A healthy diet has a number of benefits that you may not even be aware of.  Proper nutrition can improve the well-being of individuals who are both sick and healthy, so it is a good idea to make some changes as soon as possible.

Many people may claim that the right diet can actually be a cure for cancer.  While thousands believe this to be true, it is more important to realize that proper nutrition will help you on your journey to wellness while undergoing routine cancer treatments.  Cancer treatments, such as those that accompany mesothelioma, will leave you feeling sick and drained.  The right diet will help to get you on your feet by boosting your energy levels throughout the day.  You may even be surprised to see how much energy you have after incorporating the right meal plan into your life.

Another benefit of a high quality diet that many people do not know is that it improves daily functions.  Good foods, like fruits and veggies, are literally packed with vitamins and essential minerals.  These vitamins are what your body needs to heal itself and support these functions.  You may notice that the right diet puts you in a better mood and gives you a sense of peace that no processed food could ever do.  Natural and wholesome foods can be added to your diet so that you are getting the recommended calories and vitamins for that particular day.

Before making changes to your current diet, you should make an appointment with your doctor to discuss these things.  While it is easy to make quick changes to a diet plan, your doctor will be able to advise you on different things that you need to avoid or get more of for that day’s consumption.  For example, most cancer patients need to have a high amount of calories each day to prevent excessive weight loss.  Only your doctor will be able to tell you how many calories is enough to support your daily functions on a regular basis.

The best thing to remember about nutrition for mesothelioma and other forms of cancer is that good foods can help you on this journey that you are taking.  Proper nutrition will help to improve energy levels, give you a sense of well-being, and help you to heal after treatments faster than living on a diet of processed junk food.  If you feel that a proper diet is the best thing for you at this point, be sure to schedule an appointment with your doctor to see what they can recommend and advise you on when it comes to making these types of changes.

For more information about the link between nutrition and health please visit Cooking for Health.

Nutrition – a game changer in global healthcare

Fierce political debate rages on both sides of the Atlantic about the rising cost of healthcare and what should be done about it.

Spending on health services in the UK has more than doubled in cash terms in the last decade, growing from £53 billion in 2000-01 to £120 billion in 2010-11; this is equivalent to an increase of around 80 per cent in real terms (1).  In England, 22 per cent of total public spending is devoted to healthcare.

In the USA, more than $2.5 trillion is spent annually on medical care.  But as recently as 1950, Americans spent only about $8.4 billion ($70 billion in today’s dollars).  After adjusting for inflation, Americans now spend as much on health care every ten days as they did in the entire year of 1950 (2).  In the USA, medical spending now represents nearly 20 per cent of gross domestic product (GDP).

The cost of health insurance continues to climb for US companies and workers, with annual family premiums growing at a pace triple that of 2010 and outpacing wage increases (3). The chairman and CEO of Starbucks, Howard Schultz, is quoted as saying that his company spends more money on insurance for its employees than it spends on coffee (4).

New legislation, large-scale reorganisation of health services, changes in insurance schemes and budget cuts are all among the radical measures being taken by governments to address this issue.

There is much less press coverage though about the real game changer with respect to reducing healthcare costs – improving nutrition and lifestyle.

Chronic or non-communicable diseases are the top cause of death worldwide, killing more than 36 million people in 2008.  Cardiovascular diseases were responsible for 48 per cent of these deaths, cancers 21 per cent, chronic respiratory diseases 12 per cent, and diabetes 3 per cent (5).

In most middle- and high-income countries non-communicable diseases were responsible for more deaths than all other causes of death combined, with almost all high-income countries reporting more than 70 per cent of total deaths due to non-communicable diseases (6).

In the UK and the USA, non-communicable diseases account for over 80 per cent of all deaths (5).

Common, preventable risk factors underlie most of these non-communicable diseases.  These risk factors are a leading cause of the death and disability burden in nearly all countries, regardless of economic development.

The leading risk factor globally for mortality is raised blood pressure (responsible for 13 per cent of deaths globally), followed by tobacco use (9 per cent), raised blood glucose (6 per cent), physical inactivity (6 per cent), and overweight and obesity (5 per cent) (7).

If we were to stop overeating, stop eating unhealthy foods, stop smoking and stop living sedentary lives, these risk factors would reduce, the prevalence of these diseases would reduce, healthcare costs would reduce and we would enjoy a greater quality of life.

Simple changes to diet and lifestyle really can make a dramatic difference to your health and well-being (8).

If you have enjoyed this post please leave your comments below.

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Works Cited

1. National Audit Office. Healthcare across the UK: A comparison of the NHS in England, Scotland, Wales and Northern Ireland. s.l. : National Audit Office, 2012.

2. Robbins, John and Robbins, Ocean. Beyond the Obamacare debate – why does healthcare cost so much? . s.l. : Fox News, 2012.

3. US Health Insurance Costs Rise. [Online] 27 September 2011. http://www.guardian.co.uk/world/2011/sep/27/us-health-insurance-costs-climb.

4. Businessweek. [Online] 21 November 2004. http://www.businessweek.com/stories/2004-11-21/online-extra-a-full-bodied-talk-with-mr-dot-starbucks.

5. World Health Organisation. Non-communicable diseases country profiles 2011.

6. —. Global status report on noncommunicable diseases 2010. . Geneva : s.n., 2011.

7. —. Global health risks: mortality and burden of disease attributable to selected major risks. . Geneva : s.n., 2009.

8. Willett, W.C. Eat, Drink and Be Healthy. New York : Free Press, 2001. ISBN 0 684 86337 5.

9. Parliamentary Office of Science and Technology. Health Behaviour. Postnote, May 2007, no. 283. 2007.

McDonald’s Map – fast food forward?

macdonalds_us_high_9_25This week photographer Stephen Von Worley set the blogosphere buzzing with his astonishing image of the distribution of the 13,000 McDonald’s fast food outlets across the United States.

Close to highways and population centres, there is apparently no escape from the Big Macs, fries, 710-calorie salads and super-sized vats of coke.

Is anywhere sacred, wondered Von Worley?

“For maximum McSparseness, we look westward, towards the deepest, darkest holes in our map: the barren deserts of central Nevada, the arid hills of southeastern Oregon, the rugged wilderness of Idaho’s Salmon River Mountains, and the conspicuous well of blackness on the high plains of northwestern South Dakota.  There, in a patch of rolling grassland, loosely hemmed in by Bismarck, Dickinson, Pierre, and the greater Rapid City-Spearfish-Sturgis metropolitan area, we find our answer.  Between the tiny Dakotan hamlets of Meadow and Glad Valley lies the McFarthest Spot: 107 miles distant from the nearest McDonald’s, as the crow flies, and 145 miles by car!”

Yesterday, Britain’s Telegraph Newspaper reported that America’s Fast Food Temple is celebrating its 30th anniversary in France by opening its 1,142nd Gallic outlet a few yards from the Louvre Museum.

“This is the last straw,” said one art historian working at the Louvre, who declined to be named. “This is the pinnacle of exhausting consumerism, deficient gastronomy and very unpleasant odours in the context of a museum.”

This echoes the sentiment of many in France who view “McDo” as the Trojan horse of globalisation and the scourge of local produce and long lunches.

Despite this, statistics suggest the battle of Le Big Macs has already been lost. France has become McDonald’s biggest market in the world outside of the US, according to the chain. While business in traditional brasseries and bistros is in freefall, the fast food group opened 30 new outlets last year in France and welcomed 450 million customers – up 11 per cent on the previous year.

British people will either be horrified or reassured to know that despite the comparatively tiny size of our islands, we still find room for an artery-busting 1,250 McDonald’s outlets.

Is it any wonder we have an obesity crisis?

 

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