Follow Your Heart Vegan Gourmet™ Cheese Alternative

My Product Clearinghouse attempts to list and give addresses for every single national and most regional milk alternative products available in the United States. It's a big job, and it's unique. That's somewhat redundant. Nobody else would be dumb enough to try to compile something this big and keep it updated.

And while I try to doublecheck everything, some mistakes do slip through. I have to rely on readers and viewers to catch me if I don't get it right.

So a thank you, an apology, and a plug for Bob Goldberg of Follow Your Heart/Earth Island, makers of Vegan Gourmet™ Cheese Alternative for letting me know that I got the URL of his website wrong. It's already corrected on my Cheeses page, and here it is again: www.followyourheart.com.

If you go to that site, you:

can visit our Online Store, where you can purchase Vegenaise, our eggless, dairy-free mayonnaise, (Original, Grapeseed Oil, Expeller Pressed or Organic), Vegan Gourmet™ Cheese Alternative (Mozzarella, Nacho, Monterey Jack, and Cheddar), as well as our Chicken Free Chicken™ vegetarian meat substitute.

What's more, Bob tells me that they'll soon be adding a vegan sour cream and cream cheese to their Vegan Gourmet line.

If there are any other corrections that need to be made on any product, send me an email at stevecarper@cs.com.

Lactose and Sugars

All lactose is sugar, but not all sugar is lactose. And that's just the start of the confusion.

When most people talk about "sugar" they're referring to sucrose, the sugar found in sugar cane and sugar beets, among other sources. Sucrose is so common that if you see just plain "sugar" in an ingredients list on a food package, it means sucrose and nothing else. Any other type of sugar has to be mentioned specifically by name, either chemical name or common name. Honey is a type of sugar, and so is high fructose corn syrup, and molasses, and a host of other sweeteners.

Lactose is a special case, because it's the one sugar that so many people have trouble digesting. Those of us who are lactose intolerant lack the enzyme called lactase which breaks the lactose down into the simpler sugars called glucose and galactose.

And that leads to an interesting question, answered by Robert L. Wolke, professor emeritus of chemistry at the University of Pittsburgh whose latest book is "What Einstein Told His Cook 2, the Sequel: Further Adventures in Kitchen Science" (W.W. Norton, 2005), in a column in the Washington Post online.

I am a public health nutritionist and often need to recommend dairy alternatives or lactose-reduced products for clients who do not digest lactose well.
Here is my question: Why are the sugar levels of milk, yogurt and lactose-free milk all the same? It seems like the yogurt should have lower levels due to the consumption of milk sugar by the culture bacteria. And lactose-free milk should certainly have lower levels because of whatever they do to take the lactose out. However, the labels of all three products read about the same in terms of sugar.

It's puzzling, but true.

According to the U.S. Department of Agriculture's National Nutrient Database for Standard Reference, whole milk contains an average of 5.25 percent lactose by weight, while unflavored whole-milk yogurt contains 4.66 percent. Presumably, then, the culture bacteria have been allowed to consume only 0.59 percent of the milk's lactose before being forcibly restrained by cooling or killed by heat. By that time, the fermentation bacteria will have converted enough lactose into lactic acid to curdle the milk to the desired consistency.

The real head-scratcher, though, is lactose-free milk. If they've taken the lactose out of it, how come it still contains about 5 percent sugar -- the same as in whole milk?
The answer is that lactose-free milk is made not by removing the lactose but by adding the enzyme lactase. Just as sucrose is made of two simple sugars bound together, lactose is made of the two simple sugars glucose and galactose, bound together. The lactase enzyme splits the lactose into its two components, which are digestible by lactose- intolerant people.

But glucose and galactose are still sugars, and the FDA requires the aggregate amount of all sugars to be listed in the Nutrition Facts chart.

Good question, good answer, and a good rest of column as well. Take time to read it all.

Dairy Symptoms May Be Neither Intolerance Nor Allergy

Ah, science. It never stops changing, never stops learning. While you have to work to keep up with it, the glory of science is that it has something new to say every single day. (For the same reason, Intelligent Design aka Creationism will always be a fraud designed to keep you stupid – it can never say anything new: all it can do is say "no" to whatever stuff science comes up with.)

Anyway, remember Dr. Laura Paajanen, author of the dissertation I summarized in A Serious Look at Lactose Intolerance and The Different Types of Dairy Allergy?

You can take a look at a summary of another piece of her research at medpagetoday.com. The original article was published in the American Journal of Clinical Nutrition. (Paajanen L et al. Cow milk not responsible for most gastrointestinal immune-like syndromes-evidence from a population-based study. American Journal of Clinical Nutrition. 2005; 82:1327-1235.)

By giving laboratory and genetic tests to people who claimed to have symptoms when eating or drinking dairy products, Paajanen found that only a tiny minority of them tested positive for either lactose intolerance or milk allergy. What's the problem, then? Possibly something that we haven't recognized before and don't fully understand:

"We conclude that food-related gastrointestinal symptoms in young adults are caused by unspecific and unknown traits of altered mucosal immune response rather than by cow milk, as is often suspected by the patient," the study authors wrote.

"We suggest that this new entity, i.e., intestinal immune-mediated disorder, may be a self-perpetuating disease with fluctuations in symptoms, they wrote. "An autoimmune characteristic of the syndrome, at least in a subgroup of the affected subjects, cannot be ruled out."

This "as-yet uncharacterized intestinal immune-mediated disorder" as Jeff Minerd, the medpagetoday writer, put it, could explain why so many of the people who write me complaining about milk have symptoms and effects that don't correspond to anything we know about intolerance or allergy.

Unfortunately, there's no advice yet about what to do if your suffer from this, or even how to test for it. But in science identifying a problem is always the crucial first step toward a solution. Keep tuned.

Yogurt One of World's Healthiest Foods

Health magazine named the five healthiest foods in the world in its current issue.

Yogurt was one of them. "Among yogurt's benefits: enhanced immunity, improved lactose intolerance, and stronger bones," the magazine said.

That's real yogurt, as made in Greece: the slightly sour natural variety, not the sugar-laden dessert that is usually found in American supermarkets. That still has some of the same health benefits, but the extra sugar can be a problem.

The other top four:

Spain: Olive Oil
Antioxidant-rich olive oil protects against heart disease.

Japan: Soy
Protein-packed soy is linked to the prevention of cancer and osteoporosis.

India: Lentils
Lentils give you protein, cholesterol-lowering soluble fiber, and lots of iron.

Korea: Kimchi
Loaded with key vitamins, kimchi contains healthy bacteria that aids digestion.

Lactose in Beer?

I'm often asked about lactose in the oddest places. And then when I do the research it turns out the places aren't so odd.

Take beer. Once upon a time brewers used to make "milk stout," by adding whey (the lactose-containing portion of milk) to the barley. The yeast used in beer doesn't ferment the lactose (unlike some of the beasties that live in your colon) so instead of sour lactic acid, you keep a sugary taste. Milk stout was a milder form of beer and also thought to be more nutritious than the regular ales, so good that it was given to nursing mothers to fortify them.

Some people say that you can't call a beer milk stout in the United States these days, but the beers are still being made - using pure lactose rather than whey - both here and in other countries. A list of American milk stouts and other types of sweet stouts can be found at the Beer Advocate site.

Now the answer you've all been waiting for. How much lactose is left in the beer? You won't be surprised to learn that it varies too much with the recipe for a definitive answer. I did a calculation from one recipe and found that it resulted in about half as much lactose as a glass of milk. Other sources say, however, that the lactose content is small for some milk stouts. If you drink for flavor and not a buzz the lactose shouldn't be a problem.

Indian Alternatives to Milk

An article in the online Hindustan Times, Dislike cow's milk? Try alternatives, gives a great summary of the varieties of non-dairy products available in India.

In addition to commercial products, such as Oatly oat milk, the article also lists various milk alternatives that people can make for themselves including their own oat milk, rice milk, Kokkoh (a rice milk of Thai origin), almond milk, and lupin milk.

One warning: the article also lists goat milk as an alternative. As I've written before (see Goat's Milk for Lactose Intolerants? No.), goat's milk has the same lactose content as cow's milk. It's the different protein composition that allows some people with dairy allergies to drink it.

Gluten-Free Store Opens

It took years for vegetarian cafés to appear in more than a couple of cities. Vegan stores are even rarer. Allergy-free shops? Almost invisible.

So it's news that an all-gluten-free store is not only operating but thriving in Clawson, MI, in the suburban Detroit region.

The Bel Cibo Marketplace was opened by Al Doyle, who nearly died before his celiac disease was diagnosed around seven years ago.

His deli, cafe and grocery

sells only gluten-free foods, from packaged breakfast cereal, soy sauce and salad dressing to glazed doughnuts, chicken potpies, salads and side dishes, and fresh-baked pizzas.

Yes, the pizzas are available with cheese and in dairy-free style with a soy substitute. So is the lasagna. Doyle is a former restaurant chef.

Most people with celiac disease do wind up lactose intolerant, because the disease damages the part of the intestine where the lactase enzyme is made.

We can only hope for the success of this store. The better it works, the more likely it'll be that others copy it and start stores and delis of their own all over the country.

Vitamite Might Not Be Around Any Longer

I've had several people ask me where their Vitamite went.

Vitamite 100 was a non-dairy milk substitute distributed by Diehl Specialties, not to be confused with various vitamin supplements that also used the Vitamite name.

The Vitamite 100 web site is no longer functioning.

I'm taking the product off of my web site unless and until I hear that it's still officially available.

The sad truth probably is that small niche products like this have an extremely difficult time competing for shelf space and simply don't create enough sales to keep them going.

You can check for other similar products on my Nondairy Milk Substitutes page in my Product Clearinghouse.

A Serious Look at Lactose Intolerance

The dissertation, MILK HYPERSENSITIVITY
Effects of Cow’s Milk and its Processing on Gastrointestinal
Symptoms and Delayed-Type Immune Responses, by Laura Paajanen, that I just wrote about in The Different Types of Dairy Allergy also has some good technical information on lactose intolerance (also called hypolactasia in some of the medical literature.

Paajanen writes:

In lactase deficiency the activity or concentration of the lactose cleaving enzyme β-galactosidase, also called lactase, in the brush border of the small intestinal mucosa is insufficient. This hypolactasia causes insufficient digestion of lactose, the major carbohydrate of milk, a phenomenon called lactose malabsorption or lactose maldigestion. As reviewed by Sahi (1994), lactose maldigestion affects approximately 60% of the world’s adult population, the prevalence varying in Europe from 2% in Scandinavia to 70% in Italy, 70-90% in South America, Africa and Asia, and reaching 100% in some Asian countries.

The forms of lactose maldigestion are 1) lactase non-persistence, 2) secondary lactose maldigestion, and 3) rare congenital lactase deficiency. In lactase non-persistence, also called adult type lactose maldigestion, lactase activity is high at birth, decreases in a genetically programmed way in childhood and adolescence, and remains low in adulthood, which is the normal physiological situation for humans and other mammals. In populations where lactase non-persistence is predominant, the loss of lactase begins soon after weaning, and vice versa – in populations with low prevalence of lactose maldigestion, it develops later in adolescence or even in early adulthood (Sahi et al. 1983, Sahi 1994). Lactase is found at the tip of the intestinal villi, and is therefore vulnerable to intestinal diseases, inflammation and chemotherapy, leading to a secondary form of lactose maldigestion. Typically, lactase activity returns after recovery from the original disease (e.g. celiac disease, Crohn’s disease, enteritis) and after the discontinuation of chemotherapy (Bode & Gudmand-Hoyer 1988, Murphy et al. 2002, Österlund et al. 2004b). A small intestinal resection may cause irreversible secondary lactose maldigestion. Congenital lactase deficiency is an extremely rare inheritable genetic defect, which is apparent immediately after birth (Savilahti et al. 1983).

Hypolactasia accompanied by clinical symptoms such as bloating, flatulence, nausea, diarrhoea, and abdominal pain is called lactose intolerance. The symptoms occur when undigested lactose passes to the large intestine, where it serves as a fermentable substrate for the microbiota and osmotically increases the flow of water into the lumen. The intensity of the symptoms depends on the amount of lactose ingested, on individual sensitivity, the rate of gastric emptying, gastrointestinal transit time, and the pattern of microbiota in the large intestine. Ingestion of 50 g lactose, the amount commonly used in clinical tolerance tests, causes symptoms in 80-100% of lactose maldigesters, whereas the ingestion of a glass of milk (200-250 ml) causes symptoms to only 30- 50% (Vesa et al. 2000). For some unknown reason, a small percentage of maldigesters remain symptom-free even after the ingestion of large amounts of lactose. Symptoms of lactose intolerance can be reduced by food and meal pattern choices and by the consumption of low-lactose and lactose-free dairy products. Total avoidance of dairy products often results in poor calcium intake and an increased risk of fractures; so lactose intolerance is associated with reduced bone mineral density and may predispose to bone fractures (Jackson & Savaiano 2001, Kudlacek et al. 2002, Obermayer-Pietsch et al. 2004). Self-described "lactose-intolerant" individuals may restrict their dairy and calcium intake without real clinical need, and are at risk of osteoporosis and bone fractures (Savaiano 2003).

Lactose digestion can be measured by direct or indirect methods (Arola 1994). The direct methods – the measurement of mucosal disaccharidases, and an intestinal perfusion technique for the exact measurement of lactose digestion – are laborious. The most widely-used indirect tests are the traditional lactose tolerance test (measurement of serum glucose), the lactose tolerance test with ethanol (measurement of serum galactose), the hydrogen breath test and the urinary galactose test. Genotyping for the C/C-13910 variant of lactase persistence/nonpersistence is a new way of determining susceptibility to adult-type hypolactasia; however, it cannot be used as a diagnostic tool to determine lactose intolerance, as the age of reduction of lactase varies (Enattah et al. 2002, Kuokkanen et al. 2003, Rasinperä et al. 2004).

(One important point: the lactose intolerance test with ethanol is not used in the United States.)

Technical, to be sure, but a strong grounding in the technical side will help you to sort out sense from nonsense when reading articles in newspapers, magazines, or online that often are so simplified by people who dion't understand the subject that they can lead to confusion.

The Different Types of Dairy Allergy

Allergy. Hypersensitivity. Which one affects you or your family? How do you distinguish between them?

I took a stab at answering this in a simple way on my web site with Lactose Intolerance versus Milk Allergy.

I know that some of you want a deeper insight on the way the body works. Fortunately, a recent dissertation has addressed this question in depth.

It's MILK HYPERSENSITIVITY
Effects of Cow’s Milk and its Processing on Gastrointestinal
Symptoms and Delayed-Type Immune Responses,by Laura Paajanen.

The dissertation is a huge (83-page) .pdf file, so those with slow connections should be warned that it might be a long download.

The background information on allergies and intolerances is more important for readers than the study itself, so that should cut down on a lot of reading.

One part that I particularly want to highlight is the section on types of allergies. There are four major types, although just two are ones you normally have to worry about, true allergies and hypersensitivities. Paajanen writes:

Allergic reactions are traditionally classified under four types of hypersensitivity reaction which may lead to tissue damage, as described by Coombs and Gell (see Britton 2002, Hay & Westwood 2002, Male 2002, Platts-Mills 2002). It is not clear whether all four types of reaction are involved in the pathogenesis of food allergy, either in the gut itself or in remote organs. More than one mechanism may be involved in any allergic reaction, but the most plausible mechanisms are IgE-mediated reactions (Type I), and the non-IgE-mediated activation of T lymphocytes (Type IV): allergies may be exclusively IgE-mediated, partially IgEmediated or exclusively cell-mediated (Sampson 2001).

Type I, immediate anaphylactic hypersensitivity is characterised by the production of IgE antibodies against foreign proteins (Platts-Mills 2002). IgE antibodies bind to high-affinity Fc_RI receptors on mast cells and basophils. When an allergen binds between two IgE antibodies, it induces degranulation of a mast cell/basophil, which leads to the rapid release of histamine and the more gradual release of other mediators such as leukotrienes and cytokines. The combined effect of these agents is to constrict smooth muscle, dilate capillaries and induce cell infiltration. This mechanism underlies the common problem of atopic allergy….

Type IV, delayed cell-mediated hypersensitivity reactions take more than 12 hours to develop (Britton 2002). T cells identify antigens, and the antigen-sensitised T cells produce cytokines and other soluble factors which mediate the hypersensitivity reaction, or else they develop cytotoxicity. Th cell-activated macrophages destroy intracellular bacteria by releasing inflammatory mediators. Activated cytotoxic T cells and natural killer cells destroy virus-infected cells and transformed human cells, i.e. cancer cells and tissue transplants. Tissue damage occurs as a result of persistent antigenic stimulation, either because of continuing infection or because of autoimmunisation. Type IV hypersensitivity has been classified under three varieties: contact hypersensitivity and tuberculin-type hypersensitivity, which both occur within 3 days of a challenge; and granulomatous hypersensitivity reactions, which develop over a period of 21-28 days and are clinically the most serious of the Type IV responses. More than one type of delayed hypersensitivity may follow a single antigenic challenge, and reactions may overlap.

One other section is also a must read.

3.1 Different types of cow’s milk allergy
CMA before school age

CMA is usually the first major food allergy, since cow’s milk rpoteins are the first source of foreign antigens massively ingested in infancy. In several large clinical trials, the cumulative prevalence of allergy to cow’s milk has been approximately 2-3% during the first years of life in the general population (Jakobsson & Lindberg 1979, Hide & Guyer 1983, Bock 1987, Høst & Halken 1990, Schrander et al. 1993, Saarinen et al. 1999). In atopic infants, however, the prevalence is up to 50% (Sampson & McCaskill 1985, Isolauri & Turjanmaa 1996, Niggemann et al. 1999). CMA has been reported even in exclusively breast-fed infants (Høst et al. 1988, Isolauri et al. 1999, Järvinen et al. 1999, Österlund et al. 2004a). The majority of paediatric patients have symptoms from two or more organ systems: approximately 50-60% have cutaneous, 50-60% gastrointestinal and 20-30% respiratory symptoms (Høst 2002). In exclusively breast-fed infants with CMA, severe atopic eczema is a predominant symptom. In infants under the age of one year, CMA is reportedly IgE-mediated in 57-64% of the cases (Vanto et al. 1999, Saarinen & Savilahti 2000). The overall prognosis of CMA in infancy is good, with a remission rate of 85 or 90% by 3 years of age (Høst & Halken 1990, Høst 2002), non-IgE-mediated reactions being the quickest to recover (Vanto et
al. 2004)….

CMA in school-aged children and adults

In most textbooks CMA is considered to be rare in adults. Only a restricted number of studies on the immunological mechanisms of adult CMA exist, supported by either double-blind, placebo controlled milk challenges or the open challenge procedure (Nørgaard & Bindslev-Jensen 1992, Nørgaard et al. 1995, Bengtsson et al. 1996b, Bengtsson et al. 1996a, Bengtsson et al. 1997, Werfel et al. 1997, Little et al. 1998, Ulanova et al. 2000, Lin et al. 2002, Magnusson et al. 2003). In recent years recovery from CMA has become a subject of controversy. Compared to the mainly IgE-mediated CMA of infants and small children, a new form of delayed-type gastrointestinal cow’s milk hypersensitivity, also known as cow’s milk sensitive enteropathy, has been described in school-aged children and adults, and it may be more common than previously thought (Bengtsson et al. 1996b, Bengtsson et al. 1996a, Bengtsson et al. 1997, Pelto et al. 1998, Pelto et al. 1999, Ulanova et al. 2000, Kokkonen et al. 2001a, Lin et al. 2002, Magnusson et al. 2003, Kokkonen et al. 2004). After childhood, reactions to milk are rarely IgE-mediated, and virtually only case reports of IgE-mediated CMA in adults exist. In one study, only 10% of the children with CMA in childhood had IgE-mediated reactions to milk protein at school age; however, half the children still reported gastrointestinal symptoms related to the ingestion of cow’s milk protein (Kokkonen et al. 2001a).

As for diagnosing allergies in infants and children:

In young infants, open controlled challenges have been shown to be reliable when performed under professional observation in a hospital (Høst & Halken 1990, Niggemann et al. 1994, Isolauri & Turjanmaa 1996). In children over 1-2 years of age and in adults, the double-blind placebo controlled food challenge is considered the gold standard for exclusion of psychological or causal reactions (Høst & Halken 1990, Niggemann et al. 1994), but is often too laborious in clinical work (Kaila et al. 2000). In patients with delayed reactions, a placebo-controlled food challenge would be the best method of diagnosis (Bindslev-Jensen et al. 2004), but this is often not practical in clinical work. In adults in particular it may be difficult to distinguish gastrointestinal allergies from other gastrointestinal symptoms such as those of lactose intolerance or irritable bowel syndrome.

In early infancy and especially in breast-fed infants who develop immediate reactions to cow’s milk, the presence of a specific elevation of IgE antibodies to cow’s milk or a skin prick test for cow’s milk may have diagnostic value. According to reports, the specificity of the skin prick test varies greatly, from 50 to 99%, and sensitivity, from 14 to 78%, when the cut-off size of the wheal diameter is set at 3 mm (Majamaa et al. 1999a, Vanto et al. 1999, Roehr et al. 2001, Saarinen et al. 2001, Strömberg 2002, Rancé 2004). In these particular studies, the atopy patch test was found to have better specificity (71 to 100%), especially in patients with skin symptoms, but its sensitivity for identifying all the disease cases was comparatively low (from 26 to 89%). When quantitatively assessed by the CAP System FEIA, cow’s milk specific IgE antibody titres of over 32 kU/l have been reported to predict IgE-mediated CMA with as high as 95% certainty in atopic patients (Sampson & Ho 1997). However, this finding was not supported by a recent study in which much higher cow’s milk-specific IgE titres (88.8 kU/l) were needed for predicting CMA with 90% probability, and the authors concluded that no meaningful predictive decision point could be calculated for predicting CMA (Celik-Bilgili et al. 2005). Skin tests are rarely useful in adults (Nørgaard & Bindslev-Jensen 1992). Increased IgA and IgG milk antibodies are not diagnostic, but merely a sign that milk has been ingested. Basophil histamine release is more frequently measured in other food allergies (Hansen et al. 2003, Østerballe et al. 2003) than in CMA (Prahl et al. 1988), and has not usually been found to be more predictive than skin prick testing or milk-specific IgE testing.

There's much more to read as well. It's a fine summary of the literature for anybody who wants more than the "allergy lite" you usually get online.

Holy Cow!

One of the silliest arguments against drinking milk is that it's somehow "unnatural," as if all the other forms of food that humans eat - and that's virtually every plant and animal in the world - are somehow designed for human consumption.

But humans have been using cows, along with all the other major domesticated milkable animals, as a food source for thousands of years.

Recently, archaeologists have found in Gohar Tepe, in the Mazandaran province in Iran, statues of cows that are at least 3000 years old, indicating that cows were being worshipped even then.


According to the Cultural Heritage News Agency, Ali Mahforouzi, head of the excavation team, said:

Some cow statues have been discovered in the archaeological excavations of Gohar Tepe, one of which is left almost intact. These sculptures which are in shape of rhytons were being used in religious ceremonies....

The statue in the picture is the only one found intact. It's about 12 inches long, 4 inches high, and 5 inches wide. It's technically known as a rhyton, which are usually used in religious places. This one shows artistic mastery.

Civilization came to this region some 5000 years ago. They understood the value of cows and their milk for those who could drink it. How have we fallen behind them?

I'm Back

Hope you didn't get worried about me because I didn't post for a while.

Nothing happened, but I did have to go out of town unexpectedly.

While I get my thoughts together for a big post, I'll put up some older stuff I had put away for a rainy day.