ifferent, paraphrased, or verbatim. “Paraphrased” was defined as some identical words with the same overall meaning.
Emergence of the National Caries Program, 1966–1967
Table 1 provides a timeline of events during the planning and launch of the NCP.
In June 1966, President Lyndon Johnson initiated a major reappraisal of National Institutes of Health (NIH) research agendas, requesting that directors of NIH institutes submit their programs’ “priorities and objectives in the national attack on disease and disability” . The NIDR Director Seymour Kreshover’s report to President Johnson in November 1966 stated that “an accelerated program of research during the next decade could reasonably provide the means for virtual eradication of dental caries” .
The threat of the NIDR’s dental research program to the sugar industry began to crystallize in July 1967, after the president praised Kreshover’s report . While it had long been known that bacteria caused tooth decay , Kreshover based his plans on the work of NIDR scientists Robert Fitzgerald and Paul Keyes, who had singled out the bacterial strain Streptococcus mutans as a major culprit in the production of acids that caused dental caries [55,56]. Research suggested that sucrose was more hazardous than other types of sugars because it caused S. mutans to form dextrans, sticky molecules that caused the bacteria to tenaciously adhere to one another in the plaque and on the tooth’s surface . The NIDR’s increased interest in S. mutans brought renewed scrutiny to sucrose consumption and dental caries risk.
In October 1967, the NIDR’s National Dental Advisory Council identified three main areas of emphasis to inform research priorities to eradicate caries: reducing the virulence of bacteria once exposed to sugars, fluoride delivery, and, of most concern to the sugar industry, dietary modification . A particular threat was research conducted by NIDR scientist Robert Stephan, initiated in the 1940s, on the “cariogenic” (decay-causing) potential of foods [58–60]. According to Stephan, as of 1966:
There have been a great many observations, discussions, and controversies published in the literature concerning the role of different foods and particularly sweets in the etiology [of dental caries]. However…there seems to be little controlled experimental proof to show which foods are cariogenic and which noncariogenic in humans. 
Stephan had initiated work to develop an animal model that could “evaluate cariogenicity and anticariogenicity of different foods and beverages that people like and commonly consume” . Based on existing research at the time, foods containing sucrose were in danger of being placed at the top of the list of harmful cariogenic products .
Industry Deflection of Attention Away from Limiting Sugar Intake
Industry position on caries control.
At least as early as 1950, SRF knew its product damaged teeth and appreciated that both the scientific evidence and the dental community favored restricting sugar intake as a key way to control caries . The 1950 SRF annual report stated:
The ultimate aim of the Foundation in dental research has been to discover effective means of controlling tooth decay by methods other than restricting carbohydrate intake. This program has both laboratory and clinical aspects.
There is evidence tending to show that carbohydrates, including sugar, and perhaps other food types, are implicated in tooth decay. There is also evidence, though less convincing, that soluble sugars may play a bigger role than starches. Besides the relatively clear evidence there are many conjectures, traditions and myths that confuse the picture.
Until recently the great majority of the dental profession had adopted the view that practical control of tooth decay could be achieved only by restriction of carbohydrates, particularly sugar in the diet. Scientific logic, nevertheless, points to many other promising possibilities and many of these are supported by preliminary laboratory observations.  (emphasis added)
The 1950 SRF annual report also shows that industry research was se