Archive for the ‘FAQ’ Category


vegemite_11082015The VEGEMITE brand has a history spanning over 90 years. Its story began in 1922 when the Fred Walker Company, which would later become Kraft Food Company, hired a young chemist to develop a spread from one of the richest known natural sources in the Vitamin B group, brewer’s yeast.

After months of laboratory tests, Dr. Cyril P Callister, Australia’s leading food technologist of the 1920s and 30s, developed a tasty, spreadable paste. It was labelled ‘Pure Vegetable Extract’.

The Spread That Could

The Fred Walker Company initiated an ingenious plan; to have the Australian public officially name their spread. A national competition was launched, offering an attractive 50 pound prize pool for finalists. Unfortunately, the name of the winning contestant was not recorded, but it was Fred Walker’s daughter who chose the winning name – VEGEMITE – out of hundreds of entries. In 1923, VEGEMITE spread graced the shelves of grocers Australia wide. “Delicious on sandwiches and toast, and improving the flavours of soups, stews and gravies,” was how the spread was first described and marketed.

The reality was that Marmite, a thick, dark English spread, already dominated the Australian market and Australians were reluctant to even try Fred Walker’s locally made product. Poor sales of VEGEMITE spread resulted in its name being changed in 1928 to ‘Parwill’. Walker was determined to emulate the success of Marmite and the logic behind the re-branding strategy was simple; “If Marmite…then Parwill.”

Walker’s innovative method of marketing was, however, unsuccessful. Parwill failed to gain momentum across the country. It would take Fred Walker 14 years of perseverance and a change back to the original VEGEMITE brand for Australians to embrace what would later become an Australian icon.

The Spread That Did

In 1937, a limerick competition with substantial prizes including Pontiac cars was just the promotion to not only encourage entries, but also sales of VEGEMITE spread nation wide. Following the successful promotion, the VEGEMITE brand gained official product endorsement from the British Medical Association in 1939 and began advertising in the British Medical Journal. Medical professionals and baby care experts were even recommending VEGEMITE spread as a Vitamin B rich, nutritionally balanced food to their patients. By 1942, exactly twenty years after it was first developed, the VEGEMITE brand had become a staple food in every Australian home and in every Australian pantry.

During World War II the Armed Forces were buying VEGEMITE spread in bulk, due to the product’s nutritional value. Fred Walker’s company had to ration VEGEMITE spread on a per capita basis across Australia in order to meet the demand. It’s well known that absence makes the heart grow fonder, and so the reduced supply of that ubiquitous VEGEMITE flavour grew in the hearts of Australians. Once World War II had ended – coupled with the post-war migrant and baby boom, VEGEMITE spread was well and truly a part of Australia’s history, and its heart.

The Song Of Australia

In 1954, a trio of bright, energetic youngsters burst into song on radio to a toe-tapping jingle named ‘Happy Little Vegemites’. Two years later, Kraft Foods developed the infectious song into a television campaign, which continued intermittently through to the late 1960s. For the next decade, Australians were informed through advertising of the nutritional benefits of VEGEMITE spread for people of all ages, and it wasn’t until the dawn of the 1980s when the original ‘Happy Little Vegemites’ commercials, re-mastered and colourised, were broadcast to an entire new generation of Australians who were offered the chance to revel in the VEGEMITE brand’s nostalgia – and have a rose placed in every cheek thanks to what has become Australia’s second, unofficial national anthem. This commercial was brought out again in 2010 to remind Australians of their love for the iconic brand.

The Spread We Love

There aren’t many products or brands that have been embraced in the same style, or with the same amount of love, as the VEGEMITE brand has been. And there are certainly not many that continue to. The world may be forever evolving but one thing that remains the same is VEGEMITE spread’s relatively unchanged recipe. It’s loved by children, teenagers and adults. It’s still consumed by our troops overseas. It’s carried in the suitcases and backpacks of Australian travellers, as a small reminder, and a small taste, of home.

There’s a reason over 22 million jars of VEGEMITE spread are sold every year and it’s because there’s no other concentrated spread out there so full of Vitamin B and nutrients, so pleasing to the palate and so intrinsically linked with Australia’s past and future as the VEGEMITE brand is.

VEGEMITE spread can be enjoyed in many ways, and is not just limited to toast and crackers. Visit our recipe section to see the varied and versatile ways you can incorporate VEGEMITE spread into your diet.

Questions and Answers

Question: What is Vegemite made from?
Answer is: What it’s made from. According to the brand, the recipe of Vegemite is relatively unchanged. … This brewer’s yeast extract is indeed a by-product of beer manufacture and, along with salt, malt extract from barley, vegetable extract and B vitamins, it’s what gives Vegemite its unique flavour.

Question: Why is Vegemite black?
Answer: Vegemite is a thick, black, salty spread made from leftover brewer’s yeast. The yeast is combined with salt, malt extract, the B vitamins thiamine, niacin, riboflavin and folate, as well as vegetable extract, giving Vegemite the unique flavor that Australians love so much

Question: What does Vegemite smell like?
Answer: But ask someone to tell you exactly what the yeasty spread smells like, and they’ll probably answer: "It smells like Vegemite". Or maybe: "It’s a sort of meaty-but-not-meat-smell". Its fragrance is certainly distinctive Vegemite doesn’t smell like anything else.


fake_meatIf you’re vegan, it’s a question you probably get from time to time. And if you’re not, it’s probably something you’ve wondered: Why do vegans eat fake meat? And the answer is simple. First, most vegans grew up eating meat, and since many family traditions center on food, vegan meat alternatives allow people to enjoy familiar dishes and some of their favorite comfort foods without compromising their values of kindness and compassion.

Second, most people don’t go vegan because they don’t like the taste of meat. By switching to vegan versions of chicken, fish, burgers, and more, you can still enjoy your favorite flavors without supporting an industry that treats animals like garbage and pollutes our water and air.

Even if vegan meat isn’t for you, there are plenty of other delicious sources of plant-based protein. But remember, vegan meat is just meat made from plants. Wheat, soy, and peas are common ingredients in these products, which are cholesterol-free and typically high in protein and fiber.

Ready to give vegan meats a shot? Here are my top picks. Be sure to try a bunch to find your favorites!

Field Roast Frankfurters
franks
Everything you want and nothing you don’t.

Beyond Meat Beefy Crumble
beef_crumbles
Delicious savory crumbles, totally free of soy and gluten!

Tofurky Hickory Smoked Deli Slices
torfunky
From Tofurky’s mouthwatering variety of deli meats that are perfect for sandwiches!

Gardein Fishless Filets
fishless
Definite crowd pleasers.

Sweet Earth Benevolent Bacon
bacon
Because bacon doesn’t have to come from a pig.


Field Roast Smoked Tomato Deli Slices
roast
Packed with flavor.

So good!


eds_pots

EDS-HT is considered the most “benign” form, that is, it’s generally not fatal, but the chronic pain, injuries, and other symptoms it causes can easily take over a person’s life. POTS is a form of dysautonomia, or dysfunction of the autonomic nervous system (ANS).

The Ehlers-Danlos syndromes are a group of connective tissue disorders that can be inherited and are varied both in how they affect the body and in their genetic causes. They are generally characterized by joint hypermobility (joints that stretch further than normal), skin hyperextensibility (skin that can be stretched further than normal), and tissue fragility.

The Ehlers-Danlos syndromes (EDS) are currently classified into thirteen subtypes. Each EDS subtype has a set of clinical criteria that help guide diagnosis; a patient’s physical signs and symptoms will be matched up to the major and minor criteria to identify the subtype that is the most complete fit. There is substantial symptom overlap between the EDS subtypes and the other connective tissue disorders including hypermobility spectrum disorders, as well as a lot of variability, so a definitive diagnosis for all the EDS subtypes when the gene mutation is known, all but hypermobile EDS (hEDS) also calls for confirmation by testing to identify the responsible variant for the gene affected in each subtype.

For those who meet the minimal clinical requirements for an EDS subtype, but who have no access to molecular confirmation; or whose genetic testing shows one (or more) gene variants of uncertain significance in the genes identified for one of the EDS subtypes; or in whom no causative variants are identified in any of the EDS-subtype-specific genes, a “provisional clinical diagnosis” of an EDS subtype can be made. These patients should be followed clinically, but alternative diagnoses and expanded molecular testing should be considered.

Please remember that an individual’s experience with an EDS is their own, and may not necessarily be the same as another person’s experience. Diagnostic criteria are meant solely to distinguish an EDS from other connective tissue disorders, and there are many more possible symptoms for each EDS than there are criteria.

What are the symptoms of Ehlers-Danlos syndromes?

Clinical manifestations of an Ehlers-Danlos syndrome are most often joint and skin related and may include:

Joints

Joint hypermobility; loose/unstable joints which are prone to frequent dislocations and/or subluxations; joint pain; hyperextensible joints (they move beyond the joint’s normal range); early onset of osteoarthritis.

Skin

Soft velvety-like skin; variable skin hyper-extensibility; fragile skin that tears or bruises easily (bruising may be severe); severe scarring; slow and poor wound healing; development of molluscoid pseudo tumors (fleshy lesions associated with scars over pressure areas).

Miscellaneous/Less Common

Chronic, early onset, debilitating musculoskeletal pain (usually associated with the Hypermobility Type); arterial/intestinal/uterine fragility or rupture (usually associated with the Vascular Type); scoliosis at birth and scleral fragility (associated with the Kyphoscoliosis Type); poor muscle tone (associated with the Arthrochalasia Type); mitral valve prolapse; and gum disease.

Each type of Ehlers-Danlos syndrome is defined as a distinct problem in connective tissue. Connective tissue is what the body uses to provide strength and elasticity; normal connective tissue holds strong proteins that allow tissue to be stretched but not beyond its limit, and then safely return that tissue to normal. Connective tissue is found throughout the body, and Ehlers-Danlos syndromes are structural problems. An analogy: If one builds a house with faulty materials, say half the necessary wood or with soft aluminum nails, it is certain there will be problems. Some problems are more likely to show up than others, but because those materials were used everywhere and are not necessarily visible, one can be surprised by where a problem shows up or how serious it is.

It is much the same thing with an Ehlers-Danlos Syndrome and connective tissue.

The connective tissue a person with EDS is built with is not structured the way it should be. With a badly-constructed or processed connective tissue, some or all of the tissue in the EDS-affected body can be pulled beyond normal limits which causes damage. Connective tissue can be found almost anywhere, in skin, muscles, tendons and ligaments, blood vessels, organs, gums, eyes, and so on.

The problems resulting from one’s body being built out of a protein that behaves unreliably can be widespread and in a wide range of severity. It shows up in places that seem unrelated until the underlying connection to an Ehlers-Danlos syndrome is recognized.

What are the types of Ehlers-Danlos syndrome?

There are thirteen defined types of Ehlers-Danlos syndrome, as well as a number of mutations identified as Ehlers-Danlos syndrome that fall outside the current system. The major types of Ehlers-Danlos syndrome are classified according to the signs and symptoms that are manifested. Each type of Ehlers-Danlos syndrome is a distinct disorder that “runs true” in a family. An individual with Vascular Ehlers-Danlos syndrome will not have a child with Classical Ehlers-Danlos syndrome.

How is an Ehlers-Danlos Syndrome diagnosed?

If you think you might have one of the Ehlers-Danlos syndromes (EDS) or hypermobility spectrum disorders (HSD), and particularly if someone in your immediate family has been diagnosed, ask your doctor if a diagnosis fits your symptoms. If they choose to, any doctor who can diagnosis a disease is able to diagnose EDS/HSD; but most likely you’ll be given a referral to a geneticist, because EDS are genetic disorders and geneticists are most adept at distinguishing between those diseases, as well as in doing any testing necessary to differentiate EDS/HSD from the more than 200 other heritable connective tissue disorders.

A diagnosis is important because, although EDS/HSD are not curable, they are treatable. Knowing the type of EDS/HSD gives you and your medical team some idea of where problems might come from and why they’re happening. When eventually there is a cure, you’ll know to use it. And as more of us are diagnosed, EDS/HSD gain the attention all of us need, increasing the likelihood of expanded research that might lead to finding that cure.

Your path to an EDS/HSD diagnosis starts with an examination. There may be physical testing: using the Beighton Scale to assess how mobile your joints are, a search for abnormal scarring and testing your skin to determine what it feels like and how much it stretches, as well as any additional tests your particular doctor feels are needed. There’s likely to be a look into your medical history to look for conditions and problems associated with EDS/HSD, and a discussion of your family to help determine if an EDS/HSD was inherited.

Diagnosis of an EDS subtype comes by finding the one that most matches your symptoms. There are clinical criteria that help guide diagnosis; your signs and symptoms will be matched up to the major and minor criteria to identify the subtype that is the most complete fit. There is substantial symptom overlap between the EDS subtypes and the other connective tissue disorders including HSD, as well as a lot of variability between them. So a definitive diagnosis for all the EDS subtypes—except for hypermobile EDS (hEDS)—also calls for confirmation by testing to identify the responsible variant for the gene affected in each subtype. These molecular testing results also provide the basis for genetic counseling for our families, guidance on treatment options for ourselves, and help in reaching research goals.

The genetic basis for hypermobile EDS is still unknown, so an hEDS (or HSD) diagnosis rests on the criteria and what your doctor finds during your examination. The hEDS criteria also established serious consideration of joint hypermobility with all related symptoms and conditions, with hEDS at one end of the spectrum. HSD can be no less consequential than hEDS, either to your health or concern for treatment.

How prevalent are Ehlers-Danlos Syndromes?

At this time, research statistics of the Ehlers-Danlos syndromes show the total prevalence as 1 in 2,500 to 1 in 5,000 people. Recent clinical experience suggests that Ehlers-Danlos syndrome may be more common. The conditions are known to affect both males and females of all racial and ethnic backgrounds.

How are Ehlers-Danlos syndromes inherited?

The two known inheritance patterns for the Ehlers-Danlos syndromes include autosomal dominant and autosomal recessive. Regardless of the inheritance pattern, we have no choice in which genes we pass on to our children.

What is the prognosis of someone with an Ehlers-Danlos Syndrome?

The prognosis depends on the type of Ehlers-Danlos syndrome and the individual. Life expectancy can be shortened for those with the Vascular Ehlers-Danlos syndrome due to the possibility of organ and vessel rupture. Life expectancy is usually not affected in the other types. There can be a wide or narrow range of severity within a family, but each person’s case of Ehlers-Danlos syndrome will be unique. While there is no cure for the Ehlers-Danlos syndromes, there is treatment for symptoms, and there are preventative measures that are helpful for most.